Taxonomy, classification, and geographic distribution of California serogroup bunyaviruses.
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Biomedical subjects
Publications and source records attributed to C H Calisher.
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Spondweni virus is a mosquito-borne flavivirus previously reported to cause human disease in Southern and West Africa. A serologically confirmed case of Spondweni virus infection in a U.S. citizen residing in Upper Volta is reported. Symptoms included fever, chills, headache, myalgia, nausea, and rash. A greyish mucoid lining was present on the posterior pharynx. The differential diagnosis included rickettsial infection, leptospirosis, typhoid fever, and numerous viral illnesses including Lassa fever. Evidence of Spondweni virus infection was also found in two other U.S. citizens residing in Gabon and Cameroon. Spondweni virus might be a cause of acute febrile illness throughout West Africa, and its presence should be considered in the differential diagnosis of febrile illness and in antibody surveys in that region.
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An 8-year-old girl living in rural southwestern Michigan experienced sudden onset of symptoms beginning with headache, dizziness and fever which rapidly progressed to central nervous system involvement with seizures and coma. Following 27 days of hospitalization her recovery was uneventful, with no apparent sequelae 15 months after discharge. Serologic studies of paired sera showed a rise in antibody to Jamestown Canyon virus, a member of the California serogroup (family Bunyaviridae). Specific IgM anti-Jamestown Canyon virus antibody was detected in sera drawn 9 days after onset. A concomitant rise in complement fixation antibody to herpesvirus was also noted. We believe this is the first reported case of encephalitis associated with Jamestown Canyon virus infection. Reasons are presented for the current inability to routinely detect infection and clinical illness caused by this virus.
Two strains of recently isolated Venezuelan equine encephalitis (VEE) complex virus from southern Brazil, avirulent for 6- to 8-week-old mice and short-haired guinea pigs, were characterized by biologic, serologic, and biochemical means. They were shown serologically to represent a single, newly recognized variant of subtype I. Two-dimensional polyacrylamide gel electrophoresis (PAGE) of ribonuclease T1 digests of viral ribonucleic acid showed considerable homology between the genomes of the new variant prototype and variant IA. Three structural proteins were visualized by discontinuous sodium dodecyl sulfate-PAGE (SDS-PAGE). Although the smallest protein of both recent isolates migrates with the capsid proteins of other subtype I viruses, the larger structural proteins of the new variants differ in molecular weight from the E1 and E2 envelope glycoproteins of the other subtype I variants. The new isolates produced peptide fragment patterns that were identical to each other, but different from the patterns of other subtype I viruses, following SDS-PaGE of dissociated virions digested with Staphylococcus aureus V8 protease. Since these two isolates were from Culex (Melanoconion) species mosquitoes and from a bat (Carollia perspicillata), were postulated that this is an enzootic VEE virus variant for which the classification IF is suggested.
In contrast to most of the arthropod-borne flaviviruses, the flaviviruses with undetermined arthropod-borne status are probably disseminated only by direct contact with excreta (saliva, urine, feces, etc.); however, as yet undescribed arthropod transmission cycles may be found for some of them. Twenty-two of these flaviviruses, including prototype and recently isolated strains, were compared. Biologic properties were defined by infectivity titrations in suckling mice and Vero, LLC-MK2, and primary Pekin duck embryo cells, and antigenic relationships were defined by complement-fixation and plaque reduction neutralization tests. An antigenic classification scheme is proposed. Antigenic and biologic properties delimit two large clusters. The first, comprising a single antigenic complex, includes those which have yet to be isolated from arthropods, but are likely to be so (Israel turkey meningoencephalitis, Koutango, Negishi and Aroa viruses). The second, encompassing five antigenic complexes, is comprised of viruses which have been isolated exclusively from rodents or bats (Saboya, Carey Island, Dakar bat, Sokuluk, Bukalasa bat, Entebbe bat, Phnom Penh bat, Modoc, Sal Vieja, Jutiapa, San Perlita, Cowbone Ridge, Rio Bravo, Apoi, Tamana bat and Montana Myotis leucoencephalitis viruses) but includes three viruses (Saboya, Sokuluk and Entebbe bat viruses) which may be arthropod-borne, as indicated by replication in mosquito cells in vitro.
Active surveillance for La Crosse infection from 1977 to 1979 revealed 12 laboratory documented cases in children from the Cherokee reservation and nearby areas of western North Carolina. The annual rate of hospitalization with La Crosse virus was isolated from two of 34 pools of male and one of 34 pools of female Aedes triseriatus mosquitoes reared from larvae collected around the residences of reservation children who had been hospitalized with encephalitis. The occurrence of the recent cases, the history of cases in 1964 and 1965, and the demonstration of antibodies to La Crosse virus in sera from second grade children collected in 1968 (2%), in 1978 (4.5%), and in high school students in 1979 (11.3%), indicate that La Crosse has persisted in the Cherokee area for at least 15 years. La Crosse infection is infrequently reported from the southeast, but this may reflect inactive surveillance. More frequent testing would reveal whether La Crosse is a significant health problem in other areas of the southeast.
Rio Grande (RG) virus, a new member of the Phlebotomus fever serogroup, was inoculated into wild wood rats (Neotoma micropus) and laboratory-reared cotton rats (Sigmodon hispidus) to determine if these potential hosts could be experimentally infected. Nine of 14 (64%) wood rats became viremic, with titers of circulating virus ranging from 10(2.3) to 10(5.3) plaque-forming units (PFU)/ml and a geometric mean titer of 10(3.7) PFU/ml. Virus was not detected in urine specimens from inoculated wood rats but was found in a single saliva specimen. RG virus was detected in the blood of 1 of 12 (8%) cotton rats. Neutralizing (N) antibody developed in 8 of 9 inoculated wood rats which survived for 30 days postinoculation and in 11 of 12 cotton rats. N antibody was still detectable in 4 of 7 wood rats which survived for 1 year, and all 7 were resistant to rechallenge with the virus, as were 3 wood rats with naturally-acquired antibody. High mortality (36%) occurred in inoculated wood rats; whereas low mortality (8%) occurred in cotton rats. The specific cause of death of the rats was not determined. Modes of transmission of the virus in nature are discussed.
An outbreak of Ross River virus infection (epidemic polyarthritis), which occurred in American Samoa between August 1979 and January 1980, is described. On the basis of a serological survey performed near the end of the epidemic, it is estimated that at least 13,500 people were infected. Ross River virus was isolated from the blood of a single polyarthritis patient. Plaque reduction neutralization tests, using this virus strain, were done on 393 human and 143 animal sera collected on Tutuila island. Over-all, 43.8% of the people sampled had evidence of infection. Sera from 100 adult residents of the same island, collected in 1972, had no Ross River antibody, suggesting recent introduction of the virus. In contrast to the human serological data, the prevalence of Ross River antibodies among animals was relatively low. Dogs and pigs had the highest rates with 20% and 15%, respectively. Results of this study suggest that the Ross River virus cycle during the epidemic in American Samoa involved primarily humans and mosquitoes with animals less frequently infected. These observations plus the recent introduction of Ross River virus into new areas of the South Pacific suggest that a major change has occurred in the epidemiology of epidemic polyarthritis.
The indirect fluorescent antibody (FA) test was evaluated for the serodiagnosis of yellow fever (YF) cases and for detection of antibodies after 17D YF vaccination. Results were compared with those of standard serological tests, reactions with heterologous flaviviral antigens were determined, and both IgM and IgG antibodies were measured. Spot slides of infected Vero cells were used as antigen substrate. In cases of primary YF infection, the FA test for IgG antibodies provided clear diagnostic results. Indirect FA tests with anti-IgG were more sensitive than the complement-fixation (CF) test and showed specificity comparable to the CF and neutralization (N) test. Cases of YF infection superimposed upon pre-existing heterologous flaviviral immunity developed broadly-crossreactive IgG antibodies. IgM antibodies were highly specific in cases of both primary infection and superinfection but were not consistently present. Most individuals without previous flaviviral exposure who received 17D vaccine failed to develop detectable antibodies by the indirect FA test; of those with pre-existing immunity, 79% developed IgG antibodies. The indirect FA test provides a simple, rapid diagnostic procedure which should be especially useful in one-site epidemiological investigations of YF outbreaks.
A newly described flavivirus was responsible for a large encephalitis epidemic in São Paulo State, Brazil. The etiologic agent, Rocio virus, was isolated from human patients and sentinel mice. The natural history of the virus is unknown although presumed to be arthropod-borne. Rocio virus was isolated from a single pool containing 19 Psorophora ferox of 47 pools (283 specimens) of this species tested. The positive pool contained 16 deplete, 2 gravid, and 2 engorged mosquitoes. No isolations were made from 2183 pools of other species. The positive pool was collected during the year of the epidemic at the same approximate time and place where vertebrate isolations were made.
The tripartite ribonucleic acid (RNA) genomes of 23 alternate isolates of La Crosse virus have been analyzed by the procedure of oligonucleotide fingerprinting. By comparison with the fingerprints of the three viral RNA species (large, medium and small) of prototype La Crosse virus, the viruses have been categorized in terms of the degree of their RNA sequence relatedness. The A type La Crosse viruses, which have been recovered from Wisconsin, Minnesota, Indiana and Ohio, have viral RNA sequences that are closely related to those of prototype La Crosse virus. The B type La Crosse viruses, which have been recovered from Minnesota, Wisconsin and Illinois, have RNA sequences which, although related, are easily distinguished from those of type A viruses. A La Crosse virus isolate obtained from Rochester, Minnesota, appears to be an intertypic type A/B recombinant, it has a small size RNA segment like those of the B type La Crosse virus isolates, but medium- and large-sized RNA species like those of the A type La Crosse virus isolates. The C type La Crosse viruses have viral RNA sequences that neither closely resemble the A or B type La Crosse viruses. They have been recovered from eastern Ohio, New York State, Texas, Georgia and North Carolina.
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Serological diagnoses of human infections with California serogroup viruses are usually made by means of complement fixation or hemagglutination inhibition tests or both. An analysis of antibody titers in sera from 128 humans with California (La Crosse) virus infections indicated that exclusive use of the complement fixation tests would have detected only 50% of the actual seroconversions, whereas hemagglutination inhibition and neutralization tests alone would have been sufficient to make the diagnosis in 79.3% and 84.8% of the cases, respectively. These and other results presented demonstrate that the complement fixation test is not sufficiently useful as a primary tool for diagnosis of La Crosse virus infections. We suggest the use of the hemagglutination inhibition test for preliminary screening of sera from individuals with suspect infections caused by California serogroup viruses. The neutralization test should then be used or confirmation and subtype identification. If hemagglutination inhibition and neutralization titers are high and stable, the complement fixation test should then be used as a last, but specific, resort.
Antigenic relationships among 24 bunyaviruses of the Simbu serogroup were determined by complement-fixation (CF), serum dilution-plaque reduction neutralization (N) and, where possible, hemagglutination-inhibition (HI) tests. By CF, three distinct complexes of closely related viruses were identified within the serogroup. Nola and Thimiri viruses, which showed little relationship with other members of the serogroup, may represent two additional complexes. N tests in Vero cells showed that individual viruses generally were distinguishable with little difficulty. Aino and Kaikalur viruses were indistinguishable by CF or N. Seven viruses showed hemagglutination activity, and antigenic relationships among these viruses by HI paralleled those established by N tests. A classification scheme, based on both CF and N test results, for the viruses of the Simbu serogroup is proposed.
Twenty-four virus strains were isolated from Aedeomyia squamipennis mosquitoes collected in Ecuador. One additional strain each was isolated from this species from Panama and ARgentina. All 26 isolates were shown to be related serologically to prototype Gamboa virus, originally isolated from Ad. squamipennis mosquitoes collected in Panama. Antigenic comparisons of eight strains, including prototype Gamboa virus, indicated the existence of four distinct viruses. Neutralization tests with sera from a variety of mammalian and avian species from Argentina provided further evidence that Gamboa serogroup viruses are transmitted between Ad. squamipennis and birds.
Tests were run on 3,198 bird sera for neutralizing antibody of Mermet virus. The birds were mostly House Sparrows (Passer domesticus) captured in the central U.S. Antibody was detected in birds from Texas, Mississippi, Tennessee, Ohio, Indiana, Illinois, and Wisconsin, but not Kentucky or Missouri. Antibody prevalence differed by location and between years in similar locations. These results confirmed the widespread activity of Mermet virus in the central U.S., suggested irregular activity of the virus, and provided the first evidence that Mermet virus activity occurs in Mississippi, Indiana, and Wisconsin. No antibody to Mermet virus was found in paired sera from 966 humans with suspected arboviral infection.