Lymphocytic Choriomeningitis Virus

There has been an upsurge of interest in lymphocytic choriomeningitis virus (LCMV) as a human pathogen and specifically as an underdiagnosed congenital infection (1,2). LCMV is a member of the Arenaviridae family of viruses. Arenaviruses have a complex life cycle involving chronic infection and shedding of the virus in rodents and episodic infections in humans (3,4). Six of the arenaviruses (Lassa, Junin, Machupo, Guanarito, Sabia, and Whiteater Arroyo virus) produce an acute and highly fatal hemmorhagic disease in humans (mortality rates 15–30%) (4). LCMV, unlike the arenoviral hemorrhagic fever viruses, produces a flulike illness and aseptic meningitis with a mortality rate of less than 1% in infected adults (2). Epidemiology studies have shown that between 7 and 11.5% of sampled rodents in varied geographic locales have serologic evidence of LCMV infection (5–8). The virus was initially recognized in the 1930s as a cause of aseptic meningitis, was implicated in approx 10% of cases of aseptic meningitis in the winter season in the 1950s, and was identified as a congenital pathogen in 1955 in Great Britain (2,9). Recent serologic studies demonstrated that between 1.7 and 5.4% of individuals tested had been infected with LCMV (antibody against LCMV at a titer >1:16 dilutions) (8,10,11). Occupational exposure, age, and lower socioeconomic status are associated with a greater likelihood of a positive test (11). Our current understanding of congenital LCMV infection is based on a limited number (26) of published case reports; therefore, the pathogenesis, incidence, attack rate, and outcome are not fully understood (1) The current understanding of congenital LCMV infection may be biased toward more clinically apparent and severe disease.