Abstract

395 SOUTH AFRICA is now reaching the advanced stages of the HIV-1 epidemic, and in 1997 more than 16% of pregnant women attending government clinics were HIV seropositive.1 There is geographical variation in the timing and severity of the epidemic within South Africa, with the northeastern region of the country (KwaZulu-Natal Province) having a prevalence of 26.92% compared with the most southern province (Western Cape), having a prevalence of only 6.29%. In a study in Cape Town, located in Western Cape Province, subtype B was associated with homosexual transmission and subtype C with heterosexual transmission.2 On the basis of the age of the epidemic and the genetic distance between gag sequences, this study suggested multiple introductions of subtype C strains into this region of South Africa. HIV subtype C has also been identified in mine workers from the north central Gauteng Province of South Africa,3 as well as in women of Durban (KwaZulu-Natal Province).4 Owing to differences in the timing of the epidemic in different regions of the country, ethnic diversity within South Africa, as well as the presence of emigrants and refugees from other African countries, it is possible that other subtypes may have been independently introduced into different regions of the country. To assess the distribution of HIV-1 subtypes in South Africa, blood samples were obtained from 107 infected individuals who originated from five major cities situated in four geographically distinct regions of the country. HIV-1 provirus was subtyped by heteroduplex mobility assay (n 5 107); seven of these samples were sequenced in the V3±V5 region and the complete gp120 was sequenced for one subtype C isolate. In addition, to assess the relationship among HIV-1 subtype C sequences from the southern African subcontinent, these sequences were compared phylogenetically with 140 published V3 (env) sequences, 105 of which were subtype C sequences originating from the southern African region. EDTA blood was obtained from a total of 107 infected individuals attending urban clinics located in four provinces of South Africa: Johannesburg (n 5 34) and Pretoria (n 5 5) (Gauteng Province); Durban (n 5 20) (KwaZulu-Natal Province); Bloemfontein (n 5 28) (Free State Province); and Cape Town (n 5 20) (Western Cape Province) (see Table 1). Samples were collected between 1994 and 1996. DNA was extracted, the 700-bp V3±V5 region was amplified by nested polymerase chain reaction (PCR), and PCR fragments were subtyped by heteroduplex mobility assays (HMA) as described.2 The 700-bp V3±V5 fragment of seven samples, and the complete gp120 region of the env gene (1600 bp) from one of these samples (ZA347TS), were cloned and sequenced as described.2

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