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Polly R Walker

Publications and source records attributed to Polly R Walker.

4 recordsLinked to original sources
PubMed2006

High specificity of V3 serotyping among human immunodeficiency virus type-1 subtype C infected patients with varying disease status and viral phenotype.

V3 serotyping is a technique for determining HIV-1 genetic subtype based on the binding of antibodies from patient sera or plasma to synthetic V3 peptides derived from subtype consensus sequences. Variation in the performance of this assay has been attributed to V3 sequence heterogeneity, the degree of which varies with patient disease progression, virus co-receptor usage, and genetic subtype. This study assessed the performance of a competitive peptide enzyme immunoassay (cPEIA) in samples from HIV-1 subtype C infected patients with varying disease profiles, including those with syncytium (SI) and non-syncytium-inducing (NSI) viruses. Out of 90 sera tested, 94.4% reacted strongly against the subtype C peptide. There was no significant difference in assay sensitivity among samples from advanced AIDS patients in which humoral immune response may be lower, nor among SI viruses which carry changes in the V3 sequence. Four samples were found to be cross-reactive with other subtypes and one acutely infected patient sample was non-reactive due to low anti-gp120 antibody titers. A significantly higher number of samples showed secondary reactivity to subtype A, compared to other subtypes (P < 0.005). In conclusion, the assay was able to identify HIV-1 subtype C infection with a high level of sensitivity (94%) irrespective of the stage of disease and therefore provides a valuable resource for the large-scale epidemiological monitoring of the spread of HIV-1 subtypes in South Africa.

Cell Line, Transformed↗
PubMed2004

Comparative population dynamics of HIV-1 subtypes B and C: subtype-specific differences in patterns of epidemic growth.

The human immunodeficiency virus (HIV) pandemic continues to grow at an alarming rate, with a further 5 million new infections in 2003. Some 3.5 million of these were in sub-Saharan Africa, where approximately 70% of the world's HIV-positive population resides. In contrast, the spread of HIV in high-income countries has slowed since its discovery in the 1980s, and in regions such as Western Europe prevalence has decreased. Here, we employ coalescent methods to compare the epidemic growth rates of two subtypes of HIV-1 with differing epidemiological profiles: subtype C, which is dominant in sub-Saharan Africa and associated with heterosexual transmission, and subtype B, the main cause of AIDS in Western Europe and North America, and which was primarily transmitted through homosexual sex and injecting drug use. We show that although both subtypes emerged at approximately the same time ( approximately 1960), they have widely differing patterns of exponential population growth. At its current growth rate the epidemic of subtype C in sub-Saharan Africa is doubling every 2.4 years, which is approximately half the rate observed during the early stages of the subtype B epidemic in Western Europe and North America. However, the subtype C growth rate is still 5-10 times greater than that estimated for the blood-borne hepatitis C virus, supporting the hypothesis that sexual transmission has been primarily responsible for the HIV epidemic in sub-Saharan Africa.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Plasmodium chabaudi: rosetting in a rodent malaria model.

Rosetting is a property of many malaria parasite species that has been linked to virulence in the major species infecting humans, Plasmodium falciparum. Here, the basic properties of rosettes in the rodent malaria laboratory model, P. chabaudi, were studied with a view to future studies on the role of rosetting in malaria parasite virulence and transmission. Rosetting occurred in 14 out of the 15 P. chabaudi clones studied, varied consistently between clones, and ranged between 9 and 37% at full parasite maturity. Rosetting frequency markedly declined after the mouse reached peak parasitemia, possibly due to host immunity. Consistent with P. falciparum and P. vivax, rosettes in P. chabaudi were disrupted by treatment with trypsin and EDTA. However, P. chabaudi rosettes were insensitive to sulfated glycoconjugates (heparin, heparan sulfate and fucoidan). The molecular basis of rosetting in P. chabaudi is unknown at present, but the results suggest that the molecules involved may differ from those in human-infecting species.

Animals↗