Objective: The aim of this study was to test the relationship between Kaposi’s sarcoma-associated herpesvirus (KSHV) phylogeny and host ethnicity at the within-country scale. Methods: KSHV genomic DNA samples were isolated from 31 patients across eleven Ugandan ethnic groups. Amino acid sequences of the ORF-K1 gene were used to construct a neighbor-joining phylogenetic tree. Results: A5 and B1 variants predominated with no evidence of distinct ethnic or geographic distribution. A new K1 subtype (F) was identified in a member of the Bantu Gisu tribe and a new subtype B variant (B3) among members of the Bantu Ganda tribe. Conclusions: The phylogeny may yet be structured by host ethnicity if members of Ugandan groups have convoluted biological origins, even as they identify with single tribes. An alternative possibility is that KSHV subtype evolution may have preceded major diversification of sub-Saharan Africans into ethnicities as we know them today, with ethnic groups beginning their histories already hosting multiple subtypes. A third alternative is that horizontal transmission of multiple KSHV subtypes may have broken up vertical lineages of the virus passed down within Ugandan populations.
Background-Small 233-bp or 330-bp DNA fragments of the ORF26 gene of human Kaposi's sarcoma herpesvirus (KSHV) have been used extensively to identify KSHV by PCR in clinical samples; to associate KSHV with novel diseases; and to correlate KSHV strain differences with pathogenicity.
The data confirm the high frequency of CCR5/D32 heterozygosity among Caucasians. Intermediate and low-level D32 allele frequencies among Puerto Rican Hispanics and Hawaiians could be attributed to recent European Caucasian gene flow. By contrast, the inability to detect the D32 allele among Asians and other Pacific Islander groups suggests that other mechanisms are responsible for resistance to HIV-1 infection in these populations.
This article describes the impact of sequence variation on the distribution and seroreactivity of linear antigenic epitopes in gp120 encoded in new Ugandan HIV-1 clones from subtypes A, C, and D, and in North American clones from the B subtype. A region of the env gene encoding the C2 to V5 domains was PCR amplified from the lysates of peripheral blood leukocytes or from short-term cultured isolates. Computer-assisted analyses were conducted on the amino acid sequences to determine the distribution of surface structures in gp120. Despite marked sequence diversity, eight analogous epitopes were predicted for all clades of the virus analyzed. Synthetic peptides comprising the putative principal neutralizing determinant E2[V3], and other B cell epitopes E3[V3-V4], E4[V3-V4], E7[C3], and E8[V5], from a seroprevalent Ugandan isolate, AUG06c, were tested in ELISA for antigenicity with sera from Uganda, New York, and Thailand. Variable magnitudes of seroreactivity were observed for all of the peptides tested. However, a significantly higher degree of serum cross-reactivity was detected with the V3 loop peptide. ELISA reactivities of the same serum panel indicated that V3 loop peptides containing the apical residues GPGR (clones AUG06c and BRT3) or GPGQ (CUG045 and DUG044) were more antigenic and display extensive cross-reactivity as compared to analogous peptides comprising GLGQ (DUG23c), GQGQ (DUG042), or GPWG (BRT1). BETATURN analysis of the divergent V3 loop apical residues showed a good correlation of probable beta-turn occurrence with strong seroreactivity. These findings suggest that the major antigenic specificities in the divergent clades of HIV-1 are well conserved.(ABSTRACT TRUNCATED AT 250 WORDS)
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