Serum specimens from 268 individuals who were in the general population of Montgomery County, Maryland, in 1957 were tested for antibody to rubella and rubeola. The frequency of antibody to rubella increased from approximately 35% among children 1-10 years of age to 85% in the age groups 16-25 years and older. This indicates that approximately 15% of the adults sampled were susceptible to infection with rubella. The major acquisition of rubella antibody occurred among schoolage children and was several years later than that of rubeola antibody. In all age groups the frequency of rubella antibody was consistently less than that for rubeola.
A tumor cell suspension of an explanted JC virus (JCV)-induced owl monkey glioblastoma was inoculated intracranially into four recipient juvenile owl monkeys. Twenty-eight months following inoculation one owl monkey developed a glioblastoma, which was explanted into tissue culture. DNA from both the tumor tissue and tumor cells in culture hybridized to a JCV DNA probe by Southern analysis, indicating that free, as well as integrated, viral DNA may be present. At the time of the second culture passage, viral JCV DNA was extracted from these cells and cloned into a plasmid vector. Nucleotide sequencing of the regulatory region of the cloned DNA demonstrated homology with the prototype Mad-1 strain of JCV and revealed a 19-base-pair deletion in the second 98-base-pair tandem repeat that eliminated a second TATA box. This deletion is characteristic of the Mad-4 strain of JCV, which is highly neurooncogenic. By the third culture passage, 100% of the cells were T-antigen positive. Approximately one-third of the cells in culture hybridized to a biotinylated JCV DNA probe when in situ hybridization was used, a technique that only detects high-copy-number of replicating viral sequences. By the culture passage 5 and continuing through culture passage 14, viable JC virions could be recovered. The T protein synthesized by this virus, now termed JCV-586, differed from both the Mad-1 and Mad-4 strains in that it formed a stable complex with the cellular p53 protein in the tumor cells. Also, the JCV-586 T protein reacted to several monoclonal antibodies made to the simian virus 40 T protein that were not recognized by either the Mad-1 or Mad-4 strains.
Abstract Healthy homosexual men between the ages of 21 and 65 years, from the Washington, DC (n = 162), and New York City (n = 89) areas, were studied for antibodies in the serum against cytomegalovirus (CMV), herpes simplex virus (HSV) types 1 and 2, and Epstein Barr virus (EBV) viral capsid antigen (VCA). CMV‐specific antibodies were assayed by enzyme‐linked immunosorbent assay (ELISA), anti‐HSV‐1 and ‐2 antibodies were measured by indirect hemagglutination (IHA), and antibodies to EBV VCA were measured by the immunofluorescence assay. Antibodies to human T lymphotrophic virus III (HTLV‐III) were detected by ELISA and Western blot procedures. T lymphocytes were enumerated using OKT4 monoclonal antibody. Healthy male volunteer blood donors (n = 90) matched for age range and race proportions were used as controls. The percentage of seropositive individuals in the homosexual group was higher (90–98 %) for all the viruses tested than in the control group (47–87%). Comparisons of the geometric mean titers, expressed as reciprocal serum dilutions, of seropositive individuals in homosexual (H) vs control (C) group were as follows: CMV‐IgG (ELISA) H = 1:794, C = 1:68; HSV‐1 (IHA) H = 1: 248, C = 1:14; HSV‐2 (IHA) H = 1:56, C = 1:17; EBV‐VCA (IFA) H = 1:385, C = 1:131. The homosexual group also showed a higher frequency of individuals with elevated titers than the control group. The CMV IgM antibody was prevalent in 17.7% of the homosexual group and 5% of the control group; arithmetic means for ELISA values for CMV IgM were 0.207 for the homosexual group and 0.05 for the control group. In the homosexual group, the anti‐CMV antibody titers increased with age (P = 0.01) and with numbers of sex partners (P = 0.06). Both anti‐HSV‐1 and anti‐HSV‐2 antibodies correlated with the number of sex partners (P = 0.04 and P = 0.05, respectively). Neither age nor partner number correlated with response to EBV, and no particular sex act was related to the EBV VCA titer level. HTLV‐III seropositivity was associated with higher herpes virus group antibody titers, probably because of life style cofactors. Among the HTLV‐111‐seropositive subjects, those with ≤ 400 T‐helper lymphocytes/mm 3 had lower antibody titers than those with ≥ 400 T‐helper lymphocytes/mm 3 counts, suggesting an impaired immune response secondary to immunosuppression.
RELIABLE information concerning the association of clinical illness with the higher-numbered adenoviruses (Types 19 through 28) has been extremely limited. Only 1 case of documented illness has been reported.1 The following case of infection with adenovirus Type 22 provided an opportunity to follow the clinical and laboratory course of this infection.Clinical SummaryA 22-year-old female laboratory technician inadvertently sprayed a small quantity of tissue-culture fluid containing adenovirus Type 22 in her left eye on June 30, 1961. She immediately washed her face and eye with running tap water and took particular care to avoid contamination of her right eye. . . .
Cytomegalovirus (CMV) infections occur worldwide and are responsible for severe damage to the child in from one to five newborns per 20,000 births. Animal models of congenital CMV infection resulting in disease have been developed in mice and guinea pigs. We report here the development of ventricular dilatation and leptomeningitis in rhesus monkeys, Macaca mulatta, following intrauterine infection with rhesus cytomegalovirus (RCMV). Central nervous system (CNS) lesions were associated with low cytomegalovirus fluorescent antibody titers in affected fetuses. In several infected animals, RCMV was isolated at necropsy from neural and nonneural tissues taken shortly after birth. This model allows investigators to study the pathogenesis and prevention of CNS changes following RCMV infection.
We have initiated a study to identify host proteins which interact with the regulatory region of the human polyomavirus JC (JCV), which is associated with the demyelinating disease, progressive multifocal leukoencephalopathy. We examined the interaction of nuclear proteins prepared from different cell lines with the JCV regulatory region by DNA binding gel retardation assays. Binding was detected with nuclear extracts prepared from human fetal glial cells, glioma cells, and HeLa cells. Little or no binding was detected with nuclear extracts prepared from human embryonic kidney cells. Competitive binding assays suggest that the nuclear factor(s) which interacted with the JCV regulatory region was different from those which interacted with the regulatory region of the closely related polyomavirus SV40. We found three areas in the JCV regulatory region protected from DNase I digestion: site A, located just upstream from the TATA sequence in the first 98-base pair (bp) repeat; site B, located upstream from the TATA sequence in the second 98-bp repeat; and site C, located just following the second 98-bp repeat. There were some differences in the ability of the nuclear factor(s) from the two brain cell lines and HeLa cells to completely protect the nucleotides within the footprint region. The results from the DNase I protective studies and competitive DNA binding studies with specific oligonucleotides, suggest that nuclear factor-1 or a nuclear factor-1-like factor is interacting with all three sites in the JCV regulatory region. In addition, the results suggest that the nuclear factor which interacts with the JCV regulatory region from human brain cell lines is different from the factor found in HeLa cells.
