Lymphocytic Choriomeningitis Virus Antibody Research Articles

Prevalence and Risk Factors for Lymphocytic Choriomeningitis Virus Infection in Continental Croatian Regions.

Lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen associated with aseptic meningitis, severe systemic infections in immunocompromised persons, and congenital anomalies. Data on the prevalence of LCMV infections are scarce. We analyzed the seroprevalence of LCMV in continental Croatian regions. A total of 338 serum samples of professionally exposed (forestry workers, hunters, agriculture workers in contact with rodents) and non-exposed populations (general population, pregnant women) were tested for the presence of LCMV antibodies using indirect immunofluorescence assay. No participants reported recent febrile disease. LCMV IgG antibodies were detected in 23/6.8% of participants: 9.8% exposed persons and 5.1% non-exposed persons (6.1% in the general population and 3.9% in pregnant women). No participants were LCMV IgM positive. Although higher seropositivity was found in males compared to females (8.9% vs. 4.7%), inhabitants of suburban/rural areas compared to inhabitants of urban areas (9.2% vs. 4.6%), and persons who used well as a source of water compared to those who used tap (11.4% vs. 5.6%), these differences did not reach statistical significance. Results of logistic regression showed that the presence of rodents in the house/yard and cleaning rodent nests were associated with an elevated risk for LCMV infection (OR = 2.962, 95% CI = 1.019–8.607).

The impact of illegal waste sites on a transmission of zoonotic viruses

BackgroundIllegal waste disposal impacts public health and causes aesthetic and environmental pollution. Waste disposed in places without permitted and controlled facilities can provide a ready source of nutrition and shelter for rodents and thus promote the spread of their ecto- and endoparasites. The presence of two distinct zoonotic viruses, lymphocytic choriomeningitis virus (LCMV) and tick-borne encephalitis virus (TBEV), was searched at illegal waste sites. The aim of this study was to determine the prevalence of infection with both viruses in rodents and to discuss the virus-rodent relations in such environments.MethodsRodents sampled between October 2011 and April 2013 at 7 locations in the Istrian peninsula, were identified morphologically and genetically to minimize misidentification. Serological and molecular techniques were used to determine seroprevalence of infection in rodents and to detect viral RNAs. Serological testing was performed by immune fluorescence assay for detection of LCMV and TBEV specific antibodies. Real-time RT PCR was used for the detection of LCMV nucleoprotein gene and TBEV 3′ non-coding region. Data were statistically analysed using SPSS statistic v2.0.ResultsOut of 82 rodent sera tested, the presence of LCMV antibodies was demonstrated in 24.93%. The highest prevalence of LCMV infection was found in commensal Mus musculus (47.37%), followed by 11.53%, 19.04% and 25% prevalence of infection in A. agrarius, A. flavicolis and A. sylvaticus, respectively. The highest prevalence of infection in rodents (53.33%) was found in locations with large waste sites and high anthropogenic influence. LCMV seroprevalence was significantly lower in rodents sampled from natural habitats. Viral nucleic acids were screened in 46 samples but yielded no amplicons of LCMV or TBEV. In addition, TBEV specific antibodies were not detected.ConclusionsIllegal waste sites have considerable impact on the area where they are located. Results have shown that the transmission of human pathogens can be significantly increased by the presence of waste sites. However, the pathogen must be endemic in the environment where the waste site is located. The introduction of a human pathogen as a consequence of the waste site in the area of interest could not be proven.

Exposure to Lymphocytic Choriomeningitis Virus, New York, USA

To the Editor: Lymphocytic choriomeningitis virus (LCMV) is an arenavirus carried by the house mouse, Mus musculus. Human infections can range from mild febrile illness to severe encephalitis and disseminated disease (1). Infection during pregnancy is associated with teratogenic effects, including congenital hydrocephalus and chorioretinitis (2). The overall occurrence of human exposure to LCMV is not known. Two large US serosurveys suggest that 3%–5% of persons tested had previous LCMV exposure as measured by immunoglobulin (Ig) G (3,4). In 2002, LCMV-associated congenital subependymal calcifications, hydrocephalus, and chorioretinitis were confirmed for 2 children in central Syracuse, Onondaga County, New York, USA. In 2009, the Centers for Disease Control and Prevention confirmed another case of LCMV-associated congenital hydrocephalus and chorioretinitis in a child from the same neighborhood. For each of the 3 cases, the mother’s history included exposure to mice during pregnancy. One mother also had a pet guinea pig, which had negative results for LCMV by serologic testing and reverse transcription PCR of kidney tissue (5). Congenital LCMV is rarely reported to public health departments or in the literature. Therefore, to better understand the magnitude of LCMV exposure in the general population of Onondaga County, we conducted a serosurvey. The American Red Cross provided the Wadsworth Center of the New York State Department of Health with blood or serum samples collected from persons >16 years of age at blood drives during August 2009. Information about date of birth, sex, and county and ZIP code of residence was provided. A subset of samples from blood donors residing in Onondaga County were tested at the Centers for Disease and Prevention by ELISA for LCMV IgM and IgG as described (4). State and federal institutional review board approval was obtained for this study. Samples from 562 blood donors were tested. Mean age of donors was 48 years (median 50 ± 15 SD, range 17–79 years). LCMV IgG was detected in 2 (0.4%) samples (titer >400) and was undetectable in all other samples. LCMV IgM was not detected in any samples. Of the 25 donors who reported residing in 1 of the 2 ZIP codes as the case-patients with congenital LCMV, none had positive test results. Given our findings, little evidence supports a high level of human exposure to LCMV in Onondaga County. Compared with previously reported seroprevalences of 3%–5%, the proportion of persons exposed to LCMV was lower than expected (3,4). The same serologic assay was used in this study and the 2 previous US serosurveys, suggesting that the different results are not an artifact of different assays. Additionally, persons tested in the current survey were older than those tested in previous serosurveys (median 50 vs. 23 [3] and 40 years [4], respectively). Because IgG against LCMV can persist for years, seroprevalence would be expected to be higher for an older population as a result of more chances for exposure. Also, a serosurvey of >1,000 hospitalized persons from upstate New York in the 1970s detected no positive antibody titers (6), consistent with our findings. Our serosurvey had a few limitations. Blood samples from an entire county cannot detect potential household- or neighborhood-scale areas of increased risk for LCMV exposure, which may be related to focal distribution of populations of LCMV-infected house mice. Serosurveys of house mice have previously shown evidence for clustering of LCMV-infected individuals (7); however, the prevalence of LCMV in house mice in Onondaga County is unknown. Additionally, because blood donors were volunteers, the population sampled did not necessarily reflect the population at risk for LCMV exposure. Despite these considerations, the low prevalence of LCMV antibodies suggests low occurrence of LCMV exposure in this population. Although little is known about frequency of human exposure and infection, LCMV seems to be rare with a propensity for inducing severe disease. LCMV infection has been associated with high incidence of clinical disease, including a pet hamster–associated outbreak in 1973–1974 that resulted in at least 181 cases and 46 hospitalizations in 12 states (8). LCMV-related disease is reportable in only 3 states (Wisconsin, Massachusetts, Arizona) and 1 city (New York, New York) and is considered to be widely undertested and underdiagnosed. A recent survey of health care providers in Connecticut found that LCMV diagnostic tests were not requested for all patients suspected to have LCMV infection (9); thus, missed diagnoses are possible. Additional studies are needed to understand the incidence of LCMV-related disease and LCMV seroprevalence in the general population (10).

Independent Lineage of Lymphocytic Choriomeningitis Virus in Wood Mice (Apodemus sylvaticus), Spain

To clarify the presence of lymphocytic choriomeningitis virus (LCMV) in Spain, we examined blood and tissue specimens from 866 small mammals. LCMV RNA was detected in 3 of 694 wood mice (Apodemus sylvaticus). Phylogenetic analyses suggest that the strains constitute a new evolutionary lineage. LCMV antibodies were detected in 4 of 10 rodent species tested.

High prevalence of antibodies to lymphocytic choriomeningitis virus in a murine typhus endemic region in Croatia

A retrospective serological survey was carried out by the indirect immunofluorescence assay (IFA) and complement fixation (CF) test in a sample of 425 healthy residents (240 females and 185 males) to investigate whether Lymphocytic choriomeningitis virus (LCMV) circulates in the rural area of the northern Croatian island of Vir, which is known to be endemic for murine typhus. The overall prevalence of LCMV antibodies detected by IFA was found to be 36% (155 out of 425) and 13% (54 out of 425) by CF. No significant difference in the LCMV seroprevalence was observed with respect to age and gender by any of the methods used. The results show that inhabitants in the area studied are clearly being exposed to LCMV and the infection of the population occurs in the first 10 years of life. Equal prevalence of IgG and especially of short-lived CF antibodies in the elderly in comparison to other age groups and children can be explained by reinfections and boosting of antibodies through permanent contact with the virus. To the best of our knowledge this study reports the first evidence of endemic LCMV in Croatia and one of the highest LCMV human prevalence reported worldwide to date. The epidemiological association between LCMV and other zoonoses which can be expected in this community as well as the etiology of summer influenza-like illness along the coastal area of Croatia has to be explored further.

Lymphocytic choriomeningitis virus: an underdiagnosed cause of congenital chorioretinitis

PURPOSE: To elucidate the role and clinical spectrum of congenital lymphocytic choriomeningitis virus infection as a cause of chorioretinopathy, congenital hydrocephalus, and macrocephaly or microcephaly in the United States. METHODS: We performed complete ophthalmologic surveys of all residents at Misericordia, a home for the severely mentally retarded in Chicago, and prospectively evaluated all patients with chorioretinitis or chorioretinal scars during a 36-month period at Children’s Memorial Hospital, also located in Chicago. Sera for patients demonstrating chorioretinal scars (a sign of intrauterine infection) were tested for Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus and lymphocytic choriomeningitis virus antibodies. RESULTS: Four of 95 patients examined at the home had chorioretinal scars, and two of these patients had normal T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers and dramatically elevated titers for lymphocytic choriomeningitis virus. Three of 14 cases of chorioretinitis at the hospital had normal T. gondii, rubella virus, cytomegalovirus, and herpes sim-plex virus titers and elevated lymphocytic choriomeningitis virus antibody titers. (A fourth case, diagnosed in 1996, was reported 2 years ago.) CONCLUSIONS: Lymphocytic choriomeningitis virus was responsible for visual loss in two of four children secondary to chorioretinitis in a population of severely retarded children. The six new cases of lymphocytic choriomeningitis virus chorioretinitis identified in these two populations over the last 3 years, compared with the total number ever reported in the United States (10 cases), suggests that lymphocytic choriomeningitis virus may be a more common cause of congenital chorioretinitis than previously believed. Because its consequences for visual and psychomotor development are devastating, we conclude that the workup for congenital chorioretinitis should include lymphocytic choriomeningitis virus serology, especially if T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers are negative.

Age distribution of lymphocytic choriomeningitis virus serum antibody in Birmingham, Alabama: evidence of a decreased risk of infection.

Lymphocytic choriomeningitis virus (LCMV) is an arenavirus that causes human disease ranging from a mild, flu-like illness to meningitis. Infections occur principally in and around the home due to contact with infected mice. Data on the incidence of LCMV infection in the United States are scarce but suggest that the risk of infection may have decreased over the past 30-40 years. To examine this hypothesis, sera from an age-stratified sample of hospital patients in Birmingham, Alabama were tested for LCMV antibody by ELISA. The overall prevalence of LCMV-specific IgG was 3.5% (56 of 1,600). The prevalence of antibody among those < 30 years of age was 0.3% (2 of 600), while the prevalence among those 30 years of age and older was 5.4% (P < 0.0001). Multiple logistic regression was used to identify risk factors for LCMV seropositivity. Age was positively associated (P < 0.0001) and socioeconomic status was negatively associated with a positive antibody test result (P < 0.03). These data are consistent with a decreased incidence of human LCMV infection in Birmingham over the past 30-40 years.

Lymphocytic choriomeningitis virus infection and house mouse (Mus musculus) distribution in urban Baltimore.

Four hundred eighty house mice (Mus musculus) were trapped primarily from urban sites in Baltimore, Maryland from 1984 to 1989 and tested for antibody to lymphocytic choriomeningitis virus (LCMV). The majority of mice (95%) were trapped in residences at two city locations (n = 260), or in an urban park (n = 196); five additional sites were sampled. Overall, 9.0% of the mice were LCMV antibody positive and infected animals were obtained from six of eight sites, including all three of the primary city sites, where the prevalence varied significantly (3.9-13.4%). The location with the highest prevalence was an inner city residential site where positive mice were found significantly clustered within blocks and households. In this location, LCMV antibody prevalence was also significantly correlated with estimates of mouse density within individual blocks. The focal nature of LCMV infection in house mice may result from contact or vertical transmission of virus in conjunction with the highly structured social system of mice, which promotes inbreeding and limited dispersal.

Seroepidemiological survey of lymphocytic choriomeningitis virus in wild house mouse(Mus musculus)in Yokohama Port, Japan.

From 1985 to 1989, a total of 129 mice was captured from 7 piers of Yokohama port. Of these, 9 (7.0%) were positive to lymphocytic choriomeningitis virus (LCMV) antigen in indirect fluorescence antibody test. Six out of 31 mice (19.4%) in 1985 and 3 out of 23 mice (13.0%) captured in 1986 were positive. All the mice (74) captured in 1988 and 1989 were negative. Although 7 out of 17 mice (41.2%) in Osanbashi-Shinko pier and 2 out of 23 (8.7%) in Honmoku pier were positive in 1985 and 1986, all mice captured in other piers were negative. This is the first report detecting LCMV antibody in wild house mice in Japan.

Susceptibility and resistance of inbred strains of Syrian golden hamsters (Mesocricetus auratus) to wasting disease caused by lymphocytic choriomeningitis virus: pathogenesis of lethal and non-lethal infections.

In different strains of inbred Syrian golden hamsters (Mesocricetus auratus), the lymphocytic choriomeningitis virus (LCMV) strains WE and Armstrong (ARM) produced systemic infection with infective virus and viral antigens detected predominantly in reticuloendothelial organs. Host and virus strain-dependent fatal wasting disease also occurred. After infection with WE, all MHA and PD4 hamsters died of a progressive wasting disease and infectivity persisted in organs at relatively high titres. LSH and CB strain hamsters resisted lethal disease and totally eliminated infection. LVG and LHC strain hamsters were intermediate in susceptibility to WE; some died of wasting and had persistently infected organs, while others cleared infection and survived. ARM was avirulent causing an inapparent infection in all hamsters. LCMV antibody responses were temporally comparable for all hamsters with either lethal or non-lethal infection. Histologically, lymphoid hyperplasia and low-grade systemic perivascular mononuclear leukocyte infiltration were found in all LCMV-infected hamsters. However, non-necrotic segmental ileal changes, which included vascular congestion, minimal haemorrhage and crypt epithelial growth extension into the intestinal wall, were found in susceptible hamsters when infected with the lethal WE strain.

Susceptibility of inbred Syrian golden hamsters (Mesocricetus auratus) to lethal disease by lymphocytic choriomeningitis virus.

An acutely lethal LCMV disease model has been established in the Syrian golden hamster (Mesocricetus auratus) in which lethality and disease are dependent upon both the inbred hamster strain and the LCMV strain. Young adult inbred, male and female, hamsters were tested for lethal-disease susceptibility by lymphocytic choriomeningitis virus (LCMV) strains, WE or Armstrong (ARM). With WE inocula, PD4 and MHA inbred hamsters were highly susceptible to a wasting disease. LVG and LHC inbred hamsters were intermediate in susceptibility; some of these animals died of wasting illness, and others exhibited minimal disease and survived. CB and LSH hamsters were highly resistant to any disease by WE. Mean survival times of susceptible hamsters given lethal WE inocula approximated 2.5 weeks and were not dependent on virus dose. By 1.5 weeks after WE inoculation wasting disease signs were notable and consisted of lethargy, progressive body weight loss, and diarrhea. The LCMV strain, ARM, was avirulent for all hamster strains, causing neither death nor disease. Hamsters surviving WE or ARM inoculation appeared healthy, produced LCMV antibody, and acquired resistance to further lethal WE challenge. Despite hamster-lethality differences. WE and ARM appeared comparably immunogenic for all hamster strains, based on host antibody titers. A number of other differences between the LCMV strains were, however, noted which could be relevant to virus virulence and lethality for hamster hosts. These included guinea pig lethality, temperature sensitivity, and plaque morphology.

Detection of lymphocytic choriomeningitis virus antibody in colonies of laboratory animals in Japan.

Indirect fluorescent antibody method was applied for a detection of lymphocytic choriomeningitis virus (LCMV) antibody in colonies of laboratory animals in Japan. The results showed that the antibody exist in SPF mice (3/152, 2.2%) and conventional mice (30/539, 5.6%) with the titers ranging from 1:10 to 1:160. The antibody was also detected in 2.2% (2/89) of Syrian hamsters, and 2.9% (2/68) of Apodemus agrarius, 21.4% (3/14) of Japanese harvest mice which have been maintained as laboratory colony for several years. However, the antibody was not demonstrated in Mongolian gerbils, Suncus murinus, guinea pigs and rats, thus far. These results indicate that LCMV infection is present in laboratory animals in Japan, and pointed out the importance of microbiological monitoring for LCMV.

Serological diagnosis in children infected prenatally with lymphocytic choriomeningitis virus.

Lymphocytic choriomeningitis virus antibody was detected by immunofluorescence in sera collected 2 to 8 years after birth from six children probably infected prenatally. A neutralization test failed to detect antibodies in two of these children.

Detection of Lymphocytic Choriomeningitis Virus Antibody in Murine Sera by Immunofluorescence

An immunofluorescence technique developed for detection of antibody in murine sera to lymphocyitc choriomeningitis virus is described.

Detection of Lymphocytic Choriomeningitis Virus Antibody in Murine Sera by Immunofluorescence

An immunofluorescence technique developed for detection of antibody in murine sera to lymphocyitc choriomeningitis virus is described.