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Virus / Arenaviridae / Type:

Arenaviridae: Lymphocytic Choriomeningitis Virus (LCMV)

INDEX - INFORMATION AVAILABLE

GENERAL & REFERENCES

VIRUS STRUCTURE & IDENTIFICATION

ASSOCIATED HOST SPECIES OF VIRUS AND HAZARD / RISK

VIRUS LIFE CYCLE, TRANSMISSION, PHYSICAL/CHEMICAL FACTORS & BIOGEOGRAPHICAL - CLIMATIC RANGE

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THE FOLLOWING INFORMATION IS HELD ON THE DISEASE INFORMATION PAGE
Lymphocytic Choriomeninigitis (LCM) (Viral Disease):

  • Epidemiology, Disease Characteristics & Diagnosis
  • Treatment & Control

CLICK THIS LINK FOR Lymphocytic Choriomeninigitis (LCM)

General and References

Virus Summary

An arenavirus, found primarily in mice, but sometimes causing severe disease in nonhuman primates, particularly marmosets and tamarins, and humans.

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Alternative Names (Synonyms)

(Classification of virus types is an evolving discipline. The information in Wildpro has been carefully referenced to the source material, as far as possible. Readers requiring further clarification should consult the source materials and more recent publications. Classification information in Wildpro will be altered when clear and scientifically endorsed new information regarding taxonomic divisions becomes available to us.)

  • LCM Virus. (D267.035.w35)

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Associated Diseases

Lymphocytic Choriomeninigitis (LCM), also known as Callitrichid hepatitis (in Callitrichidae - Marmosets and Tamarins (Family)). (D267.035.w35)
Linked Diseases

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TAXA Group (where information has been collated for an entire group on a modular basis)

Parent Group

Arenaviridae (Virus Family)

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References

Species Author

Debra Bourne MA VetMB PhD MRCVS (V.w5)

Referee

Prof. Juan C. de la Torre PhD (V.w168)

References

Detailed references are provided attached to specific sections.

ORGANISATIONS

 

ELECTRONIC LIBRARY
(Further Reading)
Click image for full contents list of ELECTRONIC LIBRARY

Library

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Structure & Identification

Virus Morphology

Shape
Size
  • Arenaviridae (Virus Family)
  • 50-300 nm diameter (B81, B557.I.w1, B558.w1)
    • Mean 110-130 nm. (B557.I.w1)
  • 80-150 nm. (B222.27.w27)
  • Inside the virions are a number of 20 - 30 nm diameter electron-dense granules; these are characteristic of arenaviruses. (B557.I.w1, B558.w1)
Envelope
No. of particle polypeptides
  • Arenaviridae (Virus Family): At least four. Particles usually contain some host ribosomes (B81)
  • LCMV: 
    • 50 - 300 nm particles seen on electron microscopy. 
    • Within the virus up to eight dense granules, 20 - 30 nm diameter, can be seen; treatment with RNase leads to disappearance of these particles. (B557.I.w1)

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Virus Genome

Nucleic acid type/No. of strands
No. of Molecules / Strandedness
  • Arenaviridae (Virus Family): -ve stranded. Three molecules, linear or circular (B81)
  • Two single-stranded segments of RNA, given the designations L and S. Ribosomal 18S and ribosomal 28S RNA are also present. (B222.27.w27)
Molecular weight
Enzymes

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Viral Type Diversity (Sub-type/Subspecies)

Recognised Sub-types

Various strains of LCMV are known.

  • LCMV appears to be serologically constant, but with various strains noticeable based on pathogenicity. (B558.w1)
  • Recognised strains include, for example, WE, Armstrong strain (E-350), FA, WWS, CA 1371 strain and others. (B557.II.w2, B557.III.w3, B557.IX.w9)
  • Different strains of LCMV have been isolated from different outbreaks in non-human primates. (J20.284.w1)
  • Different strains of LCMV were isolated from different outbreaks associated with transplants in humans. (J222.354.w1)
  • Strains may differ considerably; a study found that viruses isolated from several people and hamsters associated with an outbreak in transplant patients were very closely related, with near-complete nucleotide sequence matching (> 99.5% matching, less than 0.5% divergence) for the L-segment (232 nt). Comparisons between this strain, well-characterised laboratory strains (Armstrong, WE) and strains involved in other outbreaks or human infections showed 12.1 - 24.1 % divergence. (J84.13.w2)
  • Strains passaged in cell culture may develop different frequencies of production of defective interfering particles; this can change apparent pathogenicity. (B558.w1)
  • Strains passaged in cell culture have developed varying abilities to produce plaques in cultures. (B558.w1)
  • Strains passaged by serial intracerebral inoculation have produced variants which are less pathogenic when inoculated intraperitoneally while remaining pathogenic when inoculated intracerebrally. (B558.w1)
  • In a study in Spain, three strains from Apodemus sylvaticus - Wood mouse from three different areas were closely related to one another as indicated by phylogeny, and formed a new lineage (isolated cluster), based on analysis of the nucleotides and deduced amino acid sequences of the glycoprotein and nucleocapsid protein genes and comparison to other strains. For the glycoprotein gene, there was 23.4 - 27.7% nucleotide difference from other strains and 15.9 - 19.7% amino acid difference; for the nucleoprotein gene, there was 19.8 - 22.0% nucleotide and 8.3 - 10.6% amino acid difference. [2009](J84.15.w9)
  • In southwestern France, two strains of LCMV were detected in Mus musculus - House mouse (out of seven mice from one dog kennel) and isolated. Phylogenetic analysis showed the two isolates to be closely related to each other and to represent a highly-divergent strain when compared to 26 other strains of LCMV. [2012](J279.12.w4)
  • Analysis of 29 strains of LCMV from sources varying in geographical location (several states in the USA, plus several countries in Europe) and year of collection (1933 - 2008) showed high diversity amongst the strains. (J84.16.w6)
  • Note: recently, with a variety of European rodent species found seropositive for LCMV, it has been suggested that there may actually be other, LCMV-related arenaviruses circulating among rodents in Europe. (J19.134.w1, J84.15.w2)
In vitro differences (Laboratory test: differentiation)
  • Strains can be distinguished from one another by nucleotide sequencing. (J84.13.w2)
In vivo differences (Affected animal: variation in infectivity and target species) Different strains of LCMV may vary considerably in their pathogenicity and lethality in a given species. (J71.149.w1)
  • The ME strain is hepatotropic in a variety of species including mice, guinea pigs and primates. (J117.72.w1)
  • Different strains of LCMV cause variable morbidity and mortality in hamsters (Mesocricetus auratus - Golden Hamster). While inoculation of both WE and ARM (Armstrong) strains resulted in systemic infection and development of an antibody response, WE strain caused mortality in some hamster strains, while ARM infection did not cause any lethal infections unless hamsters were first immunosuppressed. (J71.97.w1)
  • In cynomolgus monkeys (Macaca fascicularis - Crab-eating macaque) following experimental subcutaneous inoculation with LCMV WE, all inoculated individuals died. In contrast, with LCMV ARM strain, no deaths occurred. (J214.134.w1)
  • In Macaca mulatta - Rhesus macaque, the WE strain is lethal by intravenous inoculation while the ARM (Armstrong) strain does not cause clinical disease following intravenous inoculation. (J117.72.w1)
  • A strain in a colony of mice was noted to change; initially, it caused illness in mice which were infected in utero; later mice infected in utero showed no signs of disease and clinical signs were seen only in mice first infected while suckling. (J494.69.w1)
  • Different strains of LCMV cause variable morbidity and mortality in guinea pigs (Cavia porcellus - Domestic guinea pig). (J494.63.w1)

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Virus Detection and Identification

Notes
SAMPLE COLLECTION & SHIPPING:
  • Pooled liver, spleen and kidney samples are preferred for detection of virus. (B558.w1)
    • For PCR, correct choice of tissue (kidney is recommended) is important to maximise the chance of the agent being detected. Great care is needed to avoid cross-contamination of samples. Samples should be placed in sterile containers and frozen, preferably in a dry ice/alcohol bath or in liquid nitrogen, to prevent degradation of RNA by RNases, then held at or below minus 80 C. For shipment to a laboratory, samples should be placed in dry ice and sent by overnight courier. (J495.51.w2)
    • In a study in Spain, lungs, kidneys and spleens of small mammals were collected and were stored in RNAlater solution at minus 20 C; this preserves the virus and inactivates it. [2009](J84.15.w9)
  • Virus can be detected in saliva of persistently tolerant infected mice by mouth swabbing. (J83.7.w1)
ANTIBODY DETECTION:

Antibodies can be detected using a variety of serological tests including include complement fixation (CF), neutralization or indirect fluorescent antibody (IFA) as well as ELISA; IFA and ELISA can be used for IgM and IgG detection. Patterns of antigen development mean that different tests may be more appropriate for use at different stages post infection. Note: serological tests may fail to detect antibodies in persistently infected rodents; detection of viral RNA by RT-PCR may more appropriate.

  • Serology: (B244.w2)
    • Fourfold rise in titre in paired acute and convalescent serum samples. (B244.w2)
    • Presence of IgM in a serum sample. (B244.w2)
  • Appropriate serological tests include complement fixation (CF), neutralization or indirect fluorescent antibody (IFA). (B244.w2)
    • IFA is used most commonly in human medicine.
    • ELISA has been developed.
  • IFA or ELISA may be used to confirm infection. (J84.1.w1)
  • ELISA may be used for detection of IgM and IgG antibodies. (J222.354.w1)
  • IFA or ELISA may be used to detect IgM in serum or CSF. (B324.50.w50)

In non-human primates

  • Note: Due to the acute course of disease in non-human primates, many individuals do not seroconvert before death. (P1.1996.w8)
  • In one female Callithrix pygmaea - Pygmy marmoset housed with a male which died of LCMV in Dortmund Zoo, Germany, IgG of 1:10,240 and IgM of 1:160 were detected by IFA. (J20.284.w1)
  • Antibodies detected by indirect immunofluorescence (IFA): slides of Vero cells infected with Armstrong-strain LCMV, with IgM detected using fluorescein-isothiocyanate-labelled anti-human IgM and IgG detected using fluorescein-isothiocyanate-labelled anti-human IgG and anti-monkey IgG (Sigma). (J20.284.w1)
  • Antibodies in macaques have been detected using ELISA: viral antigen from serum-free culture medium of Vero cells was used to cover wells of microtitration plates. Following overnight incubation and blocking with 10% FCS in PBS, monkey serum in ten-fold dilutions is added and incubated at room temperature for two hours. Colour development is by addition of perooxidase-labelled goat anti-monkey IgG (KPL, Gaithersburg, MD, USA) at 1:2000 plus substrate solution (Turbo TMB-ELISA, Pierce, Rockford, IL, USA). (J71.149.w1)
  • Antibodies in macaques have been detected using PRNT with "a constant dose of virus, Vero cell monolayers and serial 1-log dilutions of plasma. Incubation of virus with serum was performed at 37 C for 1 h." End points were calculated as the highest dilution of serum producing 50% neutralization. (J71.149.w1)

In humans

  • IFA. This appears to be specific, with antibodies detectable in humans by IFA sooner than with CF or mouse neutralization test (within a few days after clinical signs developed) and remaining high for 300 days or more. (J93.2.w1) Antibodies can still be detected as long as three years after illness. (J216.96.w1, J323.66.w1)
  • The CF test can be used but often fails to detect infection in humans, and CF titres may decline again rapidly (J93.2.w1) so they are detectable for only a few months. (J323.66.w1)
  • Virus neutralisation antibodies in humans may be detectable by virus neutralisation test in mice only 30-60 days post infection, then remain detectable for 2-3 years. (J93.2.w1, J323.66.w1)
  • In humans: IFA or CF. In one outbreak associated with pet hamsters in New York State, three individuals had positive IFA but negative CF and two (without any illness) were CF positive but IFA negative; all others were positive by both tests (CF 1;4 - 1:32, IFA 1:8 - 1:256). (J416.232.w1)
    • IFA detects antibodies earlier than CF or neutralization tests. (J216.96.w1)
    • IFA is reliable for early detection of antibody for diagnosis shortly after infection. (J117.4.w1)
      • Considered positive if specific immunofluorescence occurs when serum is diluted 1:8. This test is recommended; in one study, none of 26 seronegative sera resulted in immunofluorescence at a 1:8 dilution, while 22 of 25 individuals with infections as far previous as ten years or more were positive and two others were questionably positive at a 1:8 serum dilution. In recent infections, a titre of 64 was found in an individual one day after onset of clinical signs. Titres may reach high levels (1:1000) then decline but remain detectable. (J117.4.w1)
    • Neutralization tests can be used for longer-term (possibly lifelong) detection of antibodies. (J117.4.w1)
    • Plaque reduction neutralization test (PRNT) gave definite positive (if low titre) results for all except one of 24 individuals with previous infection tested (PRNT 50%; positive titre if positive at a dilution of at least 1:10). In individuals with recent infection, positive results were present on day 20 in one individual, and on day 40 or greater in other individuals. (J117.4.w1) Neutralization antibody titres can also be determined by three different mouse inoculation methods - using the constant serum-variable virus method (to give a neutralization index); this is not useful for LCMV,, or the constant virus-variable serum method to give a neutralizing titre, or using a neutralization factor method, which requires only 0.1 mL serum. 
    • CF is of less value. CF titres are low and may be undetectable even in humans with recent infection. (J117.4.w1)
    • Sensitising antibody in human sera detected by a plaque reduction assay. This involves mixing equal volumes of virus with serially diluted serum, then after incubation, mixing this with antiserum against human immunoglobulin, and incubating for another 30 minutes before plating the mixture onto the cells. (J117.4.w1, J223.37.w1) 
      • In a study of 75 sera, 20 individuals were positive with titres of 640 - 10,240. All with positive titres were people who had had verified infection or had been in occupational contact with the virus. There was good correlation with a neutralization test using mice, except for one case which was positive by this test and negative by the mouse test for neutralizing antibody, suggesting the in vitro assay to be more sensitive than the mouse assay. (J223.37.w1)
      • Titres were mainly high (>1,000, when >160 is considered positive). This assay gave positive results soon after infection and tires were still positive in individuals with long-previous infection. It had high sensitivity and specificity (no false positive or false negatives in 72 sera in this study. (J117.4.w1)
  • IFA is useful for detection of antibodies in humans and can detect antibodies in mice by as soon as one week post infection. (B558.w1)

In rodents

  • In rodents: (J495.41.w1)
    • CF. Tires may be low and undetectable until the third week of infection. Once detectable they persist for the life of the host. (J495.41.w1)
    • ELISA. Detects antibody as soon as five days post infection. Recommended. (J495.41.w1)
    • IFA. This is more sensitive than the CF. (J495.41.w1)
    • NT. Low titres, declining with time. (J495.41.w1)
  • Note: the IFA can detect antibodies in mice with persistent tolerant infection. (B558.w1)
  • CF, neutralization or fluorescent antibody tests can be used. (B558.w1)

    • FA detects antibody much sooner than neutralization. (B558.w1)

    • The time to development of neutralization antibodies may be only a week in guinea pigs but a month in hamsters. (B558.w1)

    • Once neutralization antibodies develop in mice, guinea pigs or hamsters it is probable that they persist for the life of the animal. (B558.w1)

  • Note: Circulating antibodies may not be detected in persistently infected rodents. (B684.19.w19i)
ANTIGEN DETECTION:

Immunohistochemical staining can be used to detect the virus in tissue sections or in culture. RT-PCR can be used to detect viral antigens in tissues or plasma; PCR may be more reliable than serology for the detection of infected rodents, as persistently infected rodents may lack detectable antibodies. Virus may be isolated on Vero cell cultures; inoculation tests with mice or guinea pigs have also been used.

  • Immunohistochemical staining. (J222.354.w1)
    • Immunohistochemistry using a peroxidase-labelled antibody to a guinea pig strain of LCMV. This is carried out on paraffin blocks of tissue. (P1.1996.w8)
    • Infection of tissue culture cells with LCMV can be confirmed using immunofluorescence. (J20.284.w1)
  • Fluorescent antibody test on impression smears of tissues (brain, liver, spleen, kidneys). (B558.w1)
  • PCR:
    • RT-PCR has been used for the detection of LCMV antigen in plasma and in liver samples. (J80.77.w)
    • RT-PCR has been used in humans and hamster. (J222.354.w1)
    • LCMV RNA detected in frozen liver, spleen, serum and urine samples by RT-PCR, and by seminested PCR in paraffin-embedded liver and spleen from one Callithrix pygmaea - Pygmy marmoset. (J20.284.w1)
    • PCR has been used to identify infected individuals in a colony of captive-bred wild mice Mus domesticus. (J83.41.w1)
  • Virus isolation:
    • Virus isolation from CSF or blood. (B244.w2)
    • Virus may be detected by isolation on Vero cell or Vero E-6 monolayer cultures from blood, oral swabs or organ homogenates of acutely or chronically infected rodents. (B209.14.w14)
      • PRNT of the virus in Vero cells can be used to distinguish between arenaviruses. (B209.14.w14)
    • LCMV isolated by inoculation of L cells from liver and spleen of one Callithrix pygmaea - Pygmy marmoset and from serum of the Callimico goeldii - Goeldi's monkey. Infection of tissue culture cells with LCMV was confirmed using immunofluorescence. (J20.284.w1)
    • LCMV has been isolated from the CSF of several humans with meningitis due to LCMV, and occasionally from the blood of infected humans. (J216.96.w1, J496.58.w1)
    • The virus can be detected by: (B558.w1)
      • Intracerebral inoculation into weanling mice: clinical signs of ruffled coat and humped posture should develop in 4 - 7 days, possibly with clonic convulsions, and death in 6 - 12 days. Virus can then be detected in the brains by use of CF, neutralization or FAT.
      • Inoculation into the footpad of mice. This results in marked oedema, but without necrosis and generalised rash (which occur in addition to the oedema with ectromelia virus). (B558.w1)
        • Infection can be further confirmed by serological testing or by cross-protection testing. (B558.w1)
      • Inoculation into guinea pigs followed by serological or protection tests, since guinea pigs often do not develop clinical disease. (B558.w1)
      • Inoculation of cell cultures followed by examination of the culture for viral antigens using fluorescent antibody (FA) technique (infected cultures often do not develop any CPE). (B558.w1)

In rodents: (J495.41.w1)

  • Detection of infectious virus by intracerebral inoculation of mice. (J495.41.w1)
  • Detection of infectious virus in cell culture (BHK-21 or L929 mouse fibroblast cells) with detection of infected cells using IFA staining. (J495.41.w1)
  • Detection of viral antigen by immunocytochemistry (immunoperoxidase staining of tissues). (J495.41.w1)
  • Mouse antibody protection test. (J495.41.w1)
  • Detection of genome by in situ hybridization on histological sections. (J495.41.w1)
  • Oligonucleotide fingerprinting to distinguish among laboratory-adapted LCMV strains. (J495.41.w1)
Types of Techniques recorded as useful for viral identification
ANTIBODY DETECTION
  • Enzyme-linked Immunosorbent Assay (ELISA)
  • Plaque Reduction Neutralization Test (PRNT
  • Indirect Fluorescent Antibody (IFA) Assay
  • Complement Fixation Test (CF
  • Western blot
ANTIGEN DETECTION
  • Cell Culture
  • Reverse Transcriptase - Polymerase Chain Reaction (RT-PCR)
  • Direct Immunofluorescence / Immunohistochemistry

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Associated Host Species and Hazard / Risk

Definitive Host Species (Agent undergoes final stage of replication for transmission)

Notes

The main natural reservoirs for this virus are mice: Mus musculus - House mouse / Mus domesticus - Laboratory mouse. Antibodies have been detected in free-living population of several other rodent species, particularly mice and voles, but also Sciurus carolinensis - Eastern grey squirrel in the UK. In addition to mice, other pet and laboratory species include Rattus norvegicus - Brown rat, Mesocricetus auratus - Golden Hamster and Cavia porcellus - Domestic guinea pig. This virus can infect humans and a variety of non-human primates, particularly marmosets and tamarins (Callitrichidae), in which disease is often fatal, but antibodies have also been detected in Pan troglodytes - Chimpanzee, Pongo pygmaeus - Orang-utan and baboons.

Rodents
  • Mus spp. are the main hosts. (B72) The main host is Mus musculus, which occurs worldwide [the authors of this paper suggest that Mus musculus may be divided into Mus musculus, Mus domesticus and Mus castaneus; they add that "Given that the predominant species in Western Europe is M. domesticus, we suspect that the host of LCM is, therefore, M. domesticus." They also suggest that laboratory mice are Mus domesticus]. (J214.262.w1)
  • The natural host is Mus musculus - House mouse. (B558.w1)
  • "It can also replicate in hamsters and infect humans and primates (Callitrichidae). LCMV infection of humans has been significant in some urban areas with high rodent populations. It has also been reported to be acquired from pet hamsters." (B72)
  • Apodemus agrarius  (Apodemus - (Genus))
    • Antibodies were detected by IFA in 10/63 mice (16%) from central and southern Finland, 2001. (J157.132.w1)
  • Apodemus flavicollis - Yellow-necked mouse:
    • Antibodies detected in mice inoculated with spleen extract from these wild mice, after the wild mice were immunosuppressed by inoculation with ACTH. [1980](J19.84.w1)
    • Antibodies detected by IFA in 1/28 mice (4%) from Rize and 0/3 from Trabzon, Turkey. [2006](J1.42.w4)
    • Antibodies were detected in 6.1% (72 of of 1,181) individuals collected in Trentino, Northern Italy. [2006](J19.134.w1)
    • Antibodies were detected in 8.9% of 336 mice from eight trapping sites in northern Italy, 2002 and 2006. At Dos Gaggio, 205 of 2,732 serum samples from 1,717 mice trapped 2000 - 2006 were positive (7.5% of samples), with a per-year prevalence of 0.97 to 15.1%, highest in 2002. Prevalence was positively correlated with population density. (J84.15.w2)
    • Antibodies were detected by IFA in 6/105 mice (6%) from central and southern Finland, 2001. (J157.132.w1)
  • Apodemus mystaticus (Apodemus - (Genus))
    • Antibodies detected by IFA in 1/10 mice (10%) from Rize, 0/10 from Trabzon and 0/7 from Izmir, Turkey. [2006](J1.42.w4)
  • Apodemus sylvaticus - Wood mouse
    • Antibodies detected in 2/13 individuals in the UK (both seropositives were from the same site). [1980](J19.84.w1)
    • LCMV isolated from 1/440 Apodemus sylvaticus trapped in rural areas of West Germany,1960-1962 (and in 65/1,795 Mus musculus). [1979](J8.20.w1)
    • Antibodies detected by IFA in 2/72 individuals of this species (sensu lato) (3%) from Trabzon, 1/82 (1%) from Rize and 1/52 from Izmir (2%), Turkey. [2006](J1.42.w4)
    • Antibodies were not detected in five mice from eight trapping sites in northern Italy, 2002 and 2006. [2009](J84.15.w2)
    • In a study in Spain, LCMV RNA was detected (using nested RT-PCR) in 3/866 Apodemus sylvaticus and not in any other small mammals (total 866; with 833 being rodents); the three mice came from three different well-preserved natural areas of Spain: Sierra Nevada, Cabra and Grazalema; antibodies were detected in sera of one of two of these mice (serum not available from the third mouse). Antibodies to LCMV were detected by IFA in 21/356 (3.92%) Apodemus sylvaticus. [2009](J84.15.w9)
  • Arvicola scherman - Montane water vole (previously known as fossorial form of Arvicola terrestris - European water vole)
    • Antibodies were detected by IFAT in 13/50 voles (26.0%) from two populations in Eastern France, but not in any from another 10 populations. (J279.8.w2)
  • Cavia porcellus - Domestic guinea pig
    • Natural infection occurs. [1979](J8.20.w1)
    • Natural infection reported in individuals kept in the same room as infected mice, and in guinea pigs in contact with the infected guinea pigs. (J494.64.w1)
  • Clethrionomys glareolus - Bank vole (Myodes glareolus)
    • From Skomer (island off the coast of Wales, UK), antibodies detected in 4/10 individuals.  [1980](J19.84.w1)
    • Antibodies were detected in 3.3% (9 of 276) individuals collected in Trentino, Northern Italy. [2006](J19.134.w1)
    • Antibodies were detected in 7.4% of 135 individuals from eight trapping sites in northern Italy, 2002 and 2006. (J84.15.w2)
  • Mesocricetus auratus - Golden Hamster
    • Infected in utero or as neonates. [1979](J8.20.w1)
    • Natural infection occurs[1979](J8.20.w1)
    • Infected as adults. (J267.13.w1)
    • Natural infection in hamsters (all from one supplier) which appeared to be the source of an outbreak in humans in New York State. (J416.232.w1)
  • Microtus agrestis - Field vole antibodies detected in one of two individuals. [1980](J19.84.w1)
  • Microtus arvalis - Common Vole
    • Antibodies were detected in 14.3% (one of seven) individuals collected in Trentino, northern Italy. [2006](J19.134.w1)
    • Antibodies were detected in one of five mice (20%) from eight trapping sites in northern Italy, 2002 and 2006. (J84.15.w2)
  • Microtus roberti (Microtus - (Genus))
    • Antibodies detected in 0/4 individuals from Trabzon, 1/11 (9%) from Rize and 0/1 from Izmir, Turkey. [2006](J1.42.w4)
  • Microtus rossiaemeridionalis (Microtus - (Genus))
    • Antibodies detected in 1/8 individuals from Trabzon (13%), 0/7 from Rize and 0/9 from Izmir, Turkey. [2006](J1.42.w4)
  • Mus domesticus - Laboratory mouse
    • Two epizootics were confirmed in a large research facility with about 10% of tested mice found seropositive in one room. In another room, seropositive mice were found mainly in two adjacent racks, with highest percentages of seropositive mice in the bottom cages of the racks. (J240.48.w1)
  • Mus musculus - House mouse
    • LCMV isolated from 65/1,795 Mus musculus trapped in rural areas of West Germany,1960-1962 (and in 1/440 Apodemus sylvaticus). The overall prevalence of infection in wild mice was 3.6%, but in North Rhine-Westphalia it reached 34.7%, and 39% in Mus musculus trapped within a nine-month period in a 100-acre area of one village. [1979](J8.20.w1) [1979](J8.20.w1)
    • A study in a city in Argentina found antibodies to LCMV in 29/144 (20.1%) of these mice in 1998 and in an average of 9.4% during 2000 - 2003, but not in any of several other rodent species sampled. (J117.76.w1)
    • In grey mice Mus musculus - House mouse from fallow fields of the Patuxent Refuge, Maryland, USA. LCMV was recovered from a pool of organs from one group of 14 mice. Pooled sera from four of 10 groups of mice (90 mice total) contained antibodies to LCMV at titres of 1:64 to 1:128, indicating some of the mice in each of those four groups had been infected with the virus at some time. (J351.41.w2)
    • In a survey of 103 wild-caught and 51 captive-bred house mice Mus domesticus from northwest England, Seroprevalence of LCMV varied from 0 (0/17) to 14% (1/7) for recently-captured wild mice (total 1/24, 4%) and was 18/38 (47%) in captive wild-caught mice. For all the wild-caught mice together, prevalence was 31% (19/62), including 13/37 males (35%) and 8/33 females (24%). It was noted that prevalence was higher among the mice that had been held in captivity than in those recently caught. In F1 captive-bred mice, prevalence was 12/50 (24%) (4/24 (17%) of males, 8/26 (31%) females). Transmission in the captive-bred mice was considered to be related to the persistent, long-term shedding of the virus. No clinical disease was seen associated with the virus. Possible reasons suggested were: "a relatively lower infective dose than that used in experimental infection, low viral strain pathogenicity or greater disease resistance in wild mice compared with inbred laboratory strains." (J83.41.w1)
    • A study in the Community of Madrid, Spain found antibodies (IFA) in 11.7% (6/51) of Mus musculus. (J117.70.w1)
    • Antibodies were detected in 9.5% of wild house mice in north-eastern New South Wales, Australia [1993]. Antibodies were detected in mice sampled at three of the 14 trapping sites. (J1.29.w17)
    • In a study in Spain, antibodies to LCMV were detected by IFA in 2/25 (8.33%) Mus musculus. [2009](J84.15.w9)
    • In southwestern France, two strains of LCMV were detected in Mus musculus - House mouse (out of seven mice from one dog kennel) and isolated. [2012] (J279.12.w4)
  • Mus spretus - Algerian mouse (Mus - (Genus)).
    • A study in the Community of Madrid, Spain found antibodies (IFA) in 8.3% (3/36) of Mus spretus. (J117.70.w1)
    • In a study in Spain, antibodies to LCMV were detected by IFA in 1/6 (26.67%) Mus spretus. [2009](J84.15.w9)
  • Micromys minutus - Harvest mouse
  • Rattus norvegicus - Brown rat
    • Natural infection, IgG antibodies detected by ELISA in a "fancy" rat during epidemiological studies of an outbreak of LCMV in human transplant patients. (J84.13.w2)
    • Infection with clinical signs following intracerebral inoculation. (J494.63.w1)
    • In a study in Spain, antibodies to LCMV were detected by IFA in 1/21 (4.76%) Rattus norvegicus. [2009](J84.15.w9)
  • Sciurus carolinensis - Eastern grey squirrel
    • In the UK; antibodies detected (at 1:10 dilution of serum, initial testing with modified ELISA, confirmation using immunofluorescent testing) in 4/19 individuals (21%) in North Wales, UK, [2002 data]. (J3.150.w4)
Carnivores
Primates
  • Callimico goeldii - Goeldi's monkey:
    • In the USA (Denver Zoo, 1984, Sedgwick County Zoo, 1986/87) (J2.20.w6)
    • In the UK, reported 1982. (J83.16.w1)
    • In Dortmund Zoo, Germany, 2000. (J20.284.w1)
  • Callithrix argentata - Silvery marmoset (Callithrix argentata melanura - Silvery marmosets) in the UK, reported 1982. (J83.16.w1)
  • Callithrix geoffroi - Geoffroy's marmoset in the UK, 2005. (P3.2007b.w1)
  • Callithrix jacchus - Common marmoset in the USA (Buffalo Zoo, New York, 1987). (J2.20.w6)
  • Callithrix pygmaea - Pygmy marmosets
    • At Fort Worth Zoo, 1991. (J100.167.w1)
    • Three individuals in Dortmund Zoo, Germany, 1999. (J20.284.w1)
  • Colobus guereza - Black and white colobus (Cercopithecidae - Old-world monkeys (Family)) in the UK, June 2006. (P3.2007b.w1)
  • "Black-headed tamarin L.r. chrysomelas" (J2.20.w6) [Leontopithecus chrysomelas - Golden-headed lion tamarin or Leontopithecus caissara - Black-headed lion tamarin] in the USA (Buffalo Zoo, New York, 1987). (J2.20.w6)
  • Leontopithecus rosalia - Golden lion tamarin
    • Several locations in the USA, 1980-1987 (J2.20.w6)
    • At Fort Worth Zoo, 1991. (J100.167.w1)
    • Chafee Zoological Park, California, late 1995. (P1.1996.w8)
  • Macaca fascicularis - Crab-eating macaque
    • Experimental infection. (J214.134.w1)
    • Natural aerosol infection, fatal, in six of eight individuals housed in a room with infected mice. (J214.134.w1)
  • Macaca mulatta - Rhesus macaque
    • Experimental infection. (J117.67.w1)
  • Saguinus imperator - Emperor tamarin, Oklahoma City Zoo and Lincoln Park Zoo, Chicago 1986 and 1987  respectively (J2.20.w6)
  • Saguinus fuscicollis - Saddleback tamarin in the USA (California Marine World, Vallejo, 1988). (J2.20.w6)
  • Saguinus nigricollis - White-fronted tamarin in the USA (Lincoln Park Zoo, Chicago, 1987). (J2.20.w6)
  • Saguinus oedipus - Cotton-top tamarin in the UK, reported 1982. (J83.16.w1)
  • Antibodies detected in: (J2.24.w7)
    • 8/25 (32%) Leontopithecus rosalia - Golden lion tamarin from locations with a history of callitrichid hepatitis, 3/63 (4.8%) from other zoos and 0/124 individuals from the GLT reserve, Brazil.
    • 10/144 varied callitrichids and callimiconids from locations with a history of callitrichid hepatitis, 0/59 from other zoos and 0/53 from primate research centres.
    • 0/21 New World monkeys from locations with a history of callitrichid hepatitis, 1/5 (one Saki monkey) from other zoos and 0/23 from primate research centres.
    • 1/76 Old world monkeys, lemurs and apes (one Variegata variegata rubra - Red-ruffed lemur,) from locations with a history of callitrichid hepatitis, 10/126 (7.9%) from other zoos (ten Guinea babboons, Papio papio, all from one collection) and 0/11 from primate research centres.

    (J2.24.w7)

  • Antibodies detected by complement fixation test in: (J101.86.w3)
  • Antibodies detected in 3/296 sera of chimpanzees, including 2/12 in one colony. (B561.w14)
  • Antibodies detected by complement fixation in 1/17 sera of Pongo pygmaeus - Orang-utan in one location in 1963; no antibodies were detected in 28 individuals from that laboratory in 1966 and 1967 or 22 individuals in 1968. In gorillas, 0/14 sera from the same laboratory were positive in each of 1966,1967 and 1968 while in Pan troglodytes - Chimpanzee, at this laboratory 1/44 individuals were positive in 1966 only (no positives in samples taken in 1963, 1967 or 1968), while 3/40 individuals from a second laboratory and 1/40 from a third laboratory were positive and no individuals from three other locations were positive. (J545.35.w1)
  • Homo sapiens - Human
    • Two veterinarians caring for exposed callitrichids were found to be seropositive; neither individual reported any associated clinical signs. (J80.65.w1)
    • Two seropositive veterinarians: one had been bitten by an infected animal, and the other had necropsied an infected animal. (J2.24.w7)
    • Various reports indicate both asymptomatic exposure (as indicated by seroconversion) and clinical disease associated with LCMV infection in humans. (J80.69.w2)
    • In the UK, 13 human infections were reported 1949-1955. [1979](J8.20.w1)
    • In West Germany, in North Rhine-Westphalia where the prevalence in mice reached 34.7%, and 39% in Mus musculus trapped within a nine-month period in a 100-acre area of one village, only 5/83 humans (living in the village for an average of 23 years) had antibodies and just one was thought to have shown signs of infection. In other states,where the overall prevalnce in mice was 3.6%, human seroprevalence was 9.1% for 560 persons [1979](J8.20.w1)
    • Two of 32 Kenyans and 3/67 USA personnel were seropositive by complement fixation test in one study of antibodies in humans and non-human primates. (J101.86.w3)
    • A study in the city of Rio Cuarto, Argentina found 1.0 - 3.6% of individuals to be seropositive over the period 1998 - 2003; overall prevalence was 3.3%; more males were seropositive (4.6%) than females (2.6%); this was a significant difference (P<0.05). (J117.76.w1)
    • A study in the Community of Madrid, Spain found antibodies (IFA) in 7/400 serum samples (1.7%), including 7/209 females (3.3%) and 0.191 males (0%). There was a statistically significant (p = 0.02) difference in infection rates between males and females; there were no differences with respect to age, rural versus urban area of residence, or geographic distribution within the study area. (J117.70.w1
    • A study in northern Italy found antibodies to LCMV in 12/488 (2.5%) forestry workers. [2006](J19.134.w1)
    • A study in Spain detected LCMV by RT-PCR in two meningitis patients. [2012](J84.18.w2)
ORDERS recorded overall as containing Definitive Host Species (incl. Experimental, captive and free-ranging) (Not including infection unconfirmed by Laboratory diagnosis)
MAMMALS

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Intermediate Host and Vector Species (Agent uses an intermediate species for development and/or specific indirect transmission)

Notes

Not applicable.

Species ORDERS Reported (Not including infection unconfirmed by Laboratory diagnosis)
  • --

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Paratenic Species (Agent can survive on or in the species, but there is no replication or further development)

Notes
  • LCMV has been isolated from a variety of arthropods including bedbugs, cockroaches, fleas, flies, lice, midges, mites, mosquitoes and ticks. It has been suggested that such arthropods might play a role in transmission. (B282.16.w16)
Species ORDERS Reported (Not including infection unconfirmed by Laboratory diagnosis)
  • --

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Degree of Hazard (Risk to Humans / other Species)

LCMV is infectious to humans and poses a health hazard. Biosafety level 2 or 3 containment is needed for work with this virus (depending on the type of work carried out).
  • "LCMV infection of humans has been significant in some urban areas with high rodent populations. It has also been reported to be acquired from pet hamsters." (B72)
  • Studies involving this virus should take place only in laboratories "meeting the safety standards for working with class 3 agents". (B558.w1)
  • "BSL-2 practices, containment equipment, and facilities are suitable for activities utilizing known or potentially infectious body fluids, and for cell culture passage of laboratory-adapted strains. BSL-3 is required for activities with high potential for aerosol production, work with production quantities or high concentrations of infectious materials, and for manipulation of infected transplantable tumors, field isolates and clinical materials from human cases. Strains of LCMV that are shown to be lethal in nonhuman primates should be handled at BSL-3. ABSL-2 practices, containment equipment, and facilities are suitable for studies in adult mice with strains requiring BSL-2 containment. Work with infected hamsters also should be done at ABSL-3." (D382)
Biological Containment Level - USA
  • Biosafety level 3 (BSL-3)

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Virus Life Cycle, Transmission, Physical/Chemical Factors and Biogeographical - Climatic Range

Life Cycle and Transmission (General cycle of replication and mechanisms of moving between hosts and habitats)

Notes

SOURCES OF VIRUS

Mice (both wild and domestic) are the main source of infection.

  • Mice (both wild and domestic) are the main source of infection. (J100.167.w1, P1.1996.w8)
  • Infected primates appear not to be common sources of virus for infection of other individuals. (J2.24.w7, J100.167.w1)
    • A single Callithrix pygmaea - Pygmy marmoset which did not eat infected material did not become infected despite close contact with five other marmosets which died from LCMV infection. (J100.167.w1)
  • Infected primates which survive appear to clear the infection: antigens could not be detected in the livers of two seropositive tamarins which had survived outbreaks and died of unrelated causes three to four years later, (J2.24.w7)
  • Mice which have been infected congenitally or at a very early age (e.g. one day old) become tolerantly infected and remain as a source of virus. (J83.7.w1, J494.69.w1)
  • In tolerantly infected mice, virus is excreted in saliva, nasal secretions, urine and faeces. (J83.7.w1, J494.69.w1)
  • Mice infected as adults do not discharge virus for a prolonged period (unlike individuals infected in utero or as suckling pups). (J494.69.w1)
  • In hamsters (Mesocricetus auratus - Golden Hamster) infected in utero or as neonates, virus is present in saliva, sometimes for as long as 3-5 months, and in kidneys and urine for at least six months. (J8.20.w1)
  • Mesocricetus auratus - Golden Hamster infected as adults may have virus present in urine for several months. (J267.13.w1)
  • Faeces and urine of infected rodents. (J83.2.w1)
  • In one outbreak in humans in New York State, infection was associated with infected Mesocricetus auratus - Golden Hamster from a single supplier. (J416.232.w1)
  • In a Mesocricetus auratus - Golden Hamster, urinary bladder, skin, muscle, testis, CNS tissue, heart, lung, kidney, adrenal gland, salivary gland, liver, spleen and pancreas were all positive for LCMV by one or more tests (immunohistochemical staining, quantitative real-time RT-PCR and ckulture). (J222.354.w1)
  • Infected Cavia porcellus - Domestic guinea pigs (infected naturally) transmitted the virus to other guinea pigs following prolonged contact. (J494.63.w1)
  • Infected humans are not normally a source of virus. There are no reports of human-to-human transmission other than congenital infection, via organ transplantation, and in one case in a person who conducted an autopsy on an infected person. (J84.1.w1, J222.354.w1, J222.354.w2)
  • Virus is shed in excreta of infected mice and hamsters, including saliva. (B558.w1)

MECHANISMS OF SPREAD

Transmission is both vertical and horizontal, direct and indirect. In mice, congenital infection (female infected between nine days before conception and 11 days post conception) produce young with a persistent tolerant infection; congenital transmission can occur though several generations of Mesocricetus auratus - Golden Hamster. Transmission may occur by direct contact including by biting or by ingestion of an infected animal, or may occur indirectly by aerosol transmission or by contamination of scarified skin with urine or saliva from an infected individual. In humans, infection has occurred following handling of infected tissues e.g. at necropsy

  • Both vertical and horizontal transmission can occur. (J83.7.w1, J100.167.w1)
  • Both direct and indirect infection can occur. (J421.36.w1)
  • Congenital transmission occurs in mice. Mice infected early in pregnancy (between nine days before conception and 11 days post conception) produce young with a persistent tolerant infection. (J83.7.w1)
  • Congenital transmission can occur in Mesocricetus auratus - Golden Hamster for at least three generations. (J267.13.w1)
  • Transmission from an infected female Leontopithecus rosalia - Golden lion tamarin to its fetus has been documented. (J100.167.w1)
  • Transmission may occur by direct contact including by biting or by ingestion of an infected animal, or may occur indirectly by aerosol transmission or by contamination of scarified skin with urine or saliva from an infected individual. (J2.24.w7)
  • Direct transmission between littermates can occur; infection at a very young age is more likely to result in tolerant infection. (J83.7.w1)
  • LCMV can be transmitted in milk. (J83.7.w1)
  • Infection may be transmitted via actions such as grooming of one individual by another individual which could involve contact with saliva, urine or faeces of an infected individual. (J83.7.w1)
  • Transmission has occurred to a veterinarian performing a necropsy on an infected primate; the exact mechanism was not known (infection of the person involved was detected only by seroconversion). (J2.24.w7)
  • Licking of mouse pups by a persistently tolerantly infected mother may occasionally result in transmission of infection in pups of 0-2 days old, but much less likely than if the pup's skin has been broken. (J83.7.w1)
  • Transmission may occur via indirect contact involving urine or faeces containing virus contacting broken skin 9scarified, or via a puncture). (J83.7.w1)
  • In Mesocricetus auratus - Golden Hamster, individuals infected in utero or as neonates may transmit infection by biting, by contact of infected urine to broken skin, or via aerosol. (J8.20.w1)
  • In humans, by handling of infected tissues e.g. at necropsy. (J83.2.w1)
  • Indirect infection can occur; in an outbreak in New York State associated with pet hamsters, several people had not handled the hamsters, but had lived or worked in a room with one or more hamsters in. Infection was highest in households where the hamster was kept in a wire cage and lowest where it was kept in a poorly-ventilated aquarium or wooden cage. (J416.232.w1)
  • Iatrogenic spread can occur via transplantation of solid organs. (J222.354.w1, J222.354.w2)
  • Aerosol transmission occurs and is thought to be important. (J214.134.w1)
  • Direct contact with urine or urine-contaminated fomites (e.g. cage bedding), containing virus. (B558.w1)
  • Microdroplets or virus in air-borne dust particles. (B558.w1)
  • Note: marmosets and tamarins become infected by eating infected rodents; horizontal transmission between callitrichids has not been observed. (J100.167.w1)

ROUTES OF INFECTION

The main routes of infection are probably inhalation and contact of infectious virus with mucous membranes, although transmission also occurs by inoculation by biting, and by application of virus (e,g, in urine or saliva) to abraded skin. Transmission can also occur by bite and by application to abraded or intact skin. Aerosol inhalation is considered to be an important route of infection in humans infected from pet or laboratory Mesocricetus auratus - Golden Hamster. Transmission via arthropod has been carried out experimentally but does not appear to be important in natural transmission.

  • Inhalation and contact of infectious virus with mucous membranes "are probably the most frequent means of transmission." Transmission can also occur by bite and by application to abraded or intact skin. Transmission via arthropod has been carried out experimentally; it does not appear to be important in natural transmission. (B558.w1)
  • In mice, via contact of urine or saliva containing virus to scarified skin. (J83.7.w1)
  • By inoculation of saliva by bite. (J83.7.w1)
  • Oral, by ingestion of infected mice. (J100.167.w1, P1.1996.w8)
    • Callitrichids may be fed "pinky" mice (neonatal mice) as a form of protein supplementation. (J100.167.w1, P1.1996.w8)
    • Callitrichids may hunt and eat wild mice which enter their enclosures. (J20.284.w1, J100.167.w1, P1.1996.w8)
  • By inhalation. Aerosol inhalation is considered to be an important route of infection in humans infected from pet or laboratory Mesocricetus auratus - Golden Hamster; infections have not always been associated with direct contact with hamsters, and infections were more common when hamsters were maintained in wire-sided rather than solid sided cages, and (for infections associated with pets) when the hamsters were kept in common living areas. (J8.20.w1, J323.66.w1, J416.232.w1)
  • Dried excreted virus from rodents may be present in dust from cages, and can be inhaled. (J83.2.w1)
  • In hamsters, mice and guinea pigs, natural transmission, other than in utero or in neonates, normally requires injury to the epidermis. (J8.20.w1)
  • By inhalation. (J214.134.w1)

SPREAD WITHIN THE VERTEBRATE HOST

Spread in the vertebrate host depends on the route of transmission, with initial replication at the site of entry into the body followed by systemic spread which, at least in one experiment in mice, appeared to be lymphatic rather than haematogenous.

  •  In mice, following gastric inoculation, LCMV replicated first in epithelial cells of the gastric mucosa (sometimes detectable at 12 hours post inoculation), then in the spleen (detected at 24 hours), liver (by 48 hours), Peyer's patches of the ileum (72 hours), lungs, kidney and to a lesser degree brain by 96 hours. Virus was detectable in mesenteric lymph nodes by 24 hours, inguinal, cervical and popliteal lymph nodes by 72 hours after gastric inoculation. Following intravenous inoculation, virus was not detectable in the stomach at 12 hours. Dissemination appears to be by the lymphatic route rather than by haematogenous spread. (J45.151.w1)
  • Following aerosol transmission, it is thought that the lungs are the primary site of infection. (J45.151.w1, J214.134.w1)

CELL INFECTION AND VIRUS REPLICATION

Following initial binding to cellular receptions, the virion is taken into the cell in an endocytic vesicle; acidification of the endosome results in pH-mediated fusion of virion and endosomal membranes, resulting in delivery of the viral nucleocapsid into the cell. Replication is initiated in the cytoplasm; for full replication, production of S and L antigenomes (full-length complements to the genomic RNAs) is required; these act as templates for transcription of necessary messanger RNAs as well as being replication templates for new genomic RNAs. The process by which genomic RNAs, NP protein and L protein are assembled into nucleocapsids is not understood. New virions are released from infected cells mainly by budding from plasma membrane.

  • Initial binding to cellular receptor proteins depends on the GP1 portion of the glycoprotein spike, which binds to a cellular glycoprotein (molecular weight 120 - 140 kd) identified as alpha-dystroglycan. (B324.50.w50)
  • Following attachment, the virion is "taken into the cell in large, smooth-walled endocytic vesicles that do not appear to be clathrin coated." (B324.50.w50)
  • Acidification of the endosome results in pH-mediated fusion of virion and endosomal membranes, resulting in delivery of the viral nucleocapsid into the cell. GP1 dissociated from GP2 in acidic conditions which exposes the putative GP2 fusion peptide. (B324.50.w50)
  • In the cytoplasm, "replication is initiated by transcription of subgenomic, genome-complementary NP and L mRNAs by the viral L protein, an RNA-dependent RNA polymerase." (B324.50.w50)
  • As soon as two hours post infection NP mRNAs are detectable and NP protein may be detected by six to 12 hours, with L protein detected by 12 to 24 hours. (B324.50.w50)
  • For expression of GPC and Z proteins it is necessary for a full round of replication to occur with production of S and L antigenomes (full-length complements to the genomic RNAs). Once these have been produced they act as templates for transcription of the GPC and Z mRNAs as well as being replication templates for new genomic RNAs. (B324.50.w50)
    • GPC mRNA may be detected by two hours post infection, GPC polyprotein by 12 hours if there is a high multiplicity of infection).
  • Cleavage of GPC occurs 75 - 90 minutes post translation. (B324.50.w50)
  • It is presumed that genomic RNAs, NP protein and L protein are assembled into nucleocapsids, but the assembly process is not understood. Additionally, host cell ribosomes are packaged into virion particles, but the purpose of this is unknown. (B324.50.w50)
  • Interaction of NP and GP2 appears to be necessary for assembly of virions at the cell membrane. (B324.50.w50)
  • Electron-dense structures associate with the plasma membrane, after which virions bud from the cell by "pinching off" of the lipid bilayer followed by separation of the virion membrane and plasma membrane. (B324.50.w50)
  • The virus replicates and is released from infected cells mainly by budding from plasma membranes. (B557.I.w1, B558.w1)

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Chemical  Toxicities / Disinfectants

Notes Arenaviridae in general are inactivated by:
  • Rapidly inactivated by formalin, beta-propiolactone, chloramine B and hydrogen peroxide. (J550.37.w1)
  • Enveloped viruses are inactivated by many disinfectants including aldehydes, chlorines such as sodium hypochloride, iodophores, alkalis such as sodium hydroxide, alcohol (ethanol), amines such as quaternary amines and hydrogen peroxide, and to a lesser extent by phenols and quaternary ammonium compounds. (N36.Oct2005.w1)

Lymphocytic Choriomeningitis Virus has been shown to be inactivated by:

  • Detergent in trace quantities. (B557.I.w1)

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Physical Susceptibility (Inactivation)

Notes Arenaviridae are readily inactivated by:
  • Lipid solvents. (B557.I.w1, B558.w1)
  • Lipid solvents such as ether and chloroform and detergents such as sodium desoxycholate and Triton X-100. (J550.37.w1)

LCMV

  • Freezing and thawing rapidly inactivates LCMV WE strain in a protein-free medium. (B557.I.w1)
  • May be stored frozen at pH 7.5 - 8.0. (B557.I.w1)
  • Susceptible to low temperatures:
    • Storage at -60 C rapidly inactivates LCMV WE strain in a protein-free medium. (B557.I.w1)
    • Even with proteins or other protective substances present, low temperatures result in a decrease in infective virus titre: for example a 1,000-fold drop within four weeks at -20C. 
  • Ultrasonication rapidly inactivates LCMV WE in a protein-free medium. (B557.I.w1)
  • Acid (pH< 5.5). (B558.w1)
  • UV light. (B557.I.w1, B558.w1)
  • Gamma irradiation. (B558.w1)

Optimum conditions of Arenaviridae stability include: 

  • Serum, even in low concentration, or purified proteins, provides protection for the infectivity of the virus. (B557.I.w1)
  • Buffered glycerin also improves virus survival. (B557.I.w1)

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Environments - External Habitats (Biogeographical / Climate Type)

Notes
  • LCMV has been transmitted to humans in urban and rural environments, including the home, and in laboratories. (B244.w2)
Habitat Biomes where virus appears to be able replicate and transfer between species sufficiently well to become permanently established in Biome (Become Endemic)
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Distribution and Geographical Occurrence

Notes

LCMV may be found practically worldwide, wherever host rodents are present.

  • Europe, the Americas. (J84.1.w1)
  • In the USA, widespread. (J80.69.w2)
  • Worldwide except Australia (1980 data). (B222.27.w27)

Europe

  • In West Germany, the overall prevalence of infection in wild mice was 3.6%, but in North Rhine-Westphalia it reached 34.7%, and 39% in Mus musculus trapped within a nine-month period in a 100-acre area of one village. However, only 5/83 humans (living in the village for an average of 23 years) had antibodies and just one was thought to have shown signs of infection. In other states, human seroprevalence was 9.1% for 560 persons. [1979](J8.20.w1)
  • In the UK, in wild rodents and in humans. [1979](J8.20.w1)
  • Antibodies were detected in 9.5% of wild house mice Mus domesticus (Mus musculus - House mouse) in north-eastern New South Wales, Australia. [1993](J1.29.w17)
  • Antibodies were detected in 8/330 wild rodents (Apodemus and Microtus spp.) from three locations in Turkey in 2004. (J1.42.w4)
  • In Spain, LCMV appears to be widespread in rodents. [2009](J84.15.w9)
  • In southwestern France, two strains of LCMV were detected in Mus musculus - House mouse (out of seven mice from one dog kennel) and isolated. [2012](J279.12.w4)
  • Further information on findings in indivdal counties is provided above in the section Definitive Host Species.
General Regions with literature reports of virus in last three years (not including experimental)
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Authors & Referees

Authors Debra Bourne MA VetMB PhD MRCVS (V.w5)
Referee Prof. Juan C. de la Torre PhD (V.w168)

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