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A A Porter

Publications and source records attributed to A A Porter.

10 recordsLinked to original sources

Characterization of a new polyomavirus (Polyomavirus papionis-2) isolated from baboon kidney cell cultures.

Viruses with papovavirus morphology were seen in fluids from baboon kidney cell cultures on three separate occasions (isolates A, B, and C). The size of the virions, 47.9 nm, placed the virus in the polyomavirus genus. It grew well in baboon kidney and Vero cells and less well in human embryo lung (HEL) fibroblasts. The virus could not be identified as the previously described baboon polyomavirus, SA 12, or as any of the other known primate polyomaviruses BK, JC or SV 40, the non-primate viruses mouse polyoma, K, rabbit kidney vacuolating virus (RKV) or bovine polyomavirus (FRKV) by immunofluorescence, immune electron microscopy or hemagglutination inhibition (HI) tests. A rabbit antiserum to the new virus (isolate A) reacted only with the three isolates and not with the other primate polyomaviruses studied. Thirteen percent of 118 wild-caught baboons (Papio anubis) had HI antibody to the new polyomavirus and 21 percent were seropositive for SA 12; only two baboons had antibody to both viruses. These results suggest that in baboons there are two antigenically distinct polyomaviruses which circulate independently. The two viruses may also be distinguished by their hemagglutinating properties: SA 12 agglutinated erythrocytes from a wider range of species but only the newly recognized polyomavirus agglutinated baboon erythrocytes. We propose that the two baboon viruses, SA 12 and the new virus, should be named Polyomavirus papionis-1 and Polyomavirus papionis-2 respectively.

Animals↗

An indirect immunofluorescence method for detection of infectious BK virus in urine.

An indirect immunofluorescence (IF) method is described for the detection of infectious BK virus in urine within seven days in contrast to up to three months or longer using routine tissue culture. Virus is pelleted from the urine, inoculated onto pre-formed monolayers of human embryo lung (HEL) fibroblasts, and infected cells are detected in an indirect fluorescent antibody test using a human serum. The sensitivity of the IF method is 91%. Positive isolates may be confirmed as BK virus using specific rabbit antisera on the original inoculated cultures. Furthermore, a virus stock may be grown up by passage from the original culture fluids for further studies such as DNA analysis. As a broadly-reactive human serum is used for screening the cultures, other viruses which grow in HEL cells, such as CMV, may also be detected.

BK Virus↗

Detection of human polyomavirus DNA in urine specimens by hybridot assay.

A hybridot assay method using a labelled BK virus probe has been used to detect the presence of human polyomavirus DNA in 81 urine specimens from 61 patients, most of whom were immuno-compromised to some degree. Twenty-eight urines from 23 patients had detectable DNA. The results have been compared to virus isolation and electron microscopy on the same specimens. In 90 per cent a comparable result was obtained by at least one of the other two tests and in the 73 specimens on which all 3 tests were performed there was 80 per cent agreement between all. In 6 cases the hybridot assay was more sensitive in detecting infection.

Animals↗

Prospective study of the human polyomaviruses BK and JC and cytomegalovirus in renal transplant recipients.

Forty eight renal transplant recipients were investigated prospectively for evidence of infection with the polyomaviruses BK and JC and cytomegalovirus. An active polyomavirus infection was shown in 31 patients (65%) and cytomegalovirus in 30 (62.5%). Half of the BK and JC virus infections occurred within the first three months after transplantation compared with 93% of the cytomegalovirus infections. Very late polyomavirus infections two or more years after the transplant were also shown. Cytology was useful in identifying polyomavirus but not cytomegalovirus infections, and 21 (68%) of the 31 polyomavirus infected patients excreted inclusion-bearing cells. Only three patients had symptoms possibly associated with the polyomavirus infection. One patient with BK virus infection developed ureteric stenosis and a second patient had malaise and vomiting. One patient with JC virus infection developed pericarditis and effusion. Renal function became impaired at the time of the polyomavius infection in eight patients (26%) and ureteric obstruction and pericarditis developed in two patients treated with methyl prednisolone for possible rejection. At the end of the study 25 of the 31 polyomavirus infected patients (81%) had functioning renal grafts. The detection of polyomavirus infection is important as increased immunosuppression needs to be avoided to prevent possible complications such as ureteric stenosis in transplant recipients.

Adolescent↗

Human polyomavirus in pregnancy. A model for the study of defence mechanisms to virus reactivation.

We have carried out a longitudinal study of human polyomavirus infection in 71 pregnant women and correlated the virological findings with changes in the defence system in the same patients. As reactivation of human polyomaviruses generally occurred late in the second trimester it was possible to distinguish between the immunological changes which preceded the onset of reactivation and those which were secondary to the infection. Evidence of reactivation was detected in 26 women; all had high or rising antibody titres against BK or JC virus, but only five of these developed viruria. A positive correlation was observed between a high monocyte count in early pregnancy and subsequent virus reactivation. The virus excretors had significantly lower neutrophil counts than the women who had no evidence of virus reactivation. In contrast, women with serological evidence of virus activity but no viruria has significantly higher neutrophil counts than the non-activators. They also had stronger lymphocyte responses to PHA than the virus excretors. Virus activators were found to have a significant lymphopenia in the third trimester compared to the non-activators. High antibody levels did not appear to inhibit virus excretion. These findings suggest that monocytosis may predispose to reactivation of human polyomaviruses in pregnancy. On the other hand, ability to contain the virus once it has been activated, was associated with neutrophilia, and relatively vigorous in vitro reactivity of lymphocytes to PHA. Persistent lymphopenia was probably secondary to virus reactivation. The model on which this study is based could be adapted to investigate the causes of reactivation of other viruses. It may also help to identify risk factors in patients who are particularly susceptible to infection with opportunistic viruses.

Animals↗