A midcourse assessment of hantavirus pulmonary syndrome.

Our understanding of infectious diseases follows a natural course—the initial discovery of the cause, the exploration of the natural history and biology of the etiologic agent, and finally the cure or solution. The discovery of Sin Nombre virus (SNV), one of the viruses causing hantavirus pulmonary syndrome (HPS), is unparalleled in terms of the rapid progress of the scientific investigation leading to its description. A cluster of cases of fatal adult respiratory syndrome was recognized in the Four Corners region of the United States in May 1993, and within a few days serologic evidence confirmed hantavirus infection (1). The outbreak occurred in the wake of the Institute of Medicine’s report Emerging Infections: Microbial Threats to Health in the United States, in which acute respiratory disease was first on the list of clinical syndromes requiring high-priority surveillance (2). The scientific community has now entered the midcourse phase of HPS research, including the exploration of the natural history of the American hantaviruses. Seven articles in this issue describe studies of rodent reservoirs of Sin Nombre and related viruses. They illustrate the multidisciplinary nature of such studies, which require ecologic methods, in addition to the newer molecular biology techniques that have helped hantavirologists detect and characterize the viruses. These and other studies have elucidated much about the natural host relationships of hantaviruses. Multiple hantavirus genotypes exist in virtually all parts of North and South America; each hantavirus genotype has a single rodent species as its principal reservoir. Evidence exists that the virus and rodent have evolved together. Each hantavirus variant is focal in distribution. Prevalence of antibody is high in some regions, and low or absent in others, even when the same species of rodent is found in both places. Rodents are not infected at birth; they acquire the virus from other rodents. Once infected, the animals develop antibody, but many, or maybe all, infected rodents remain infected. Because of rapid turnover of the rodent population (as older antibody-carrying animals die and nonimmune animals are born), antibody prevalence can vary greatly, from 0% to 50%, with prevalence often lower than 20%. The studies also have raised new questions. Why and by what route are animals infected? The articles in this issue suggest that contamination of wounds when animals fight may be an important route of infection, while allowing for the possibility of secondary mechanisms, such as venereal transmission or close association during communal …