HTLV-2B strains, similar to those found in several Amerindian tribes, are endemic in central African Bakola Pygmies.

BACKGROUND: The presence and origin of endemic foci of human T-lymphotropic virus type 2 (HTLV2) infection in Africa remain a matter of debate. METHODS: To better appreciate such determinants, we performed a survey of 1918 inhabitants from Cameroon forest areas, including 1051 Bakola Pygmies and 867 Bantus. RESULTS: The overall HTLV-1/2 seroprevalence was 4% (49 cases of HTLV-1 and 27 cases of HTLV-2 infection). Both infections were mainly restricted to the Bakola Pygmies, with surprisingly no HTLV-2 infections in the Bantu population. Both HTLV-1 and HTLV-2 seroprevalences increased with age. There was evidence of ongoing HTLV-2 transmission in this population. Lymphoid T cell lines producing HTLV-2 were established. HTLV-2 long terminal repeat sequences (672 base pairs) obtained from 7 infected Bakola were highly similar to each other (<1% nucleotide divergence), as well as to Amerindian HTLV-2B strains. Analyses on a complete sequence (8954 base pairs) confirmed that it was a typical HTLV-2 subtype B strain. Along with molecular clock analysis, these data strongly suggest that HTLV-2 has been endemic in the Bakola Pygmy population for a long time. CONCLUSIONS: This study demonstrates clearly an HTLV-2 endemicity with ongoing transmission in an African population. Furthermore, it give insights into central questions regarding the origins and evolution rate of HTLV-2 and the migrations of infected populations.

Respective roles of serological status and blood specific antihuman herpesvirus 8 antibody levels in human herpesvirus 8 intrafamilial transmission in a highly endemic area.

Transmission of human herpesvirus 8 (HHV-8), the etiological agent of Kaposi's sarcoma, occurs mainly during childhood in endemic countries and, to a large extent, through intrafamilial contacts. To additionally investigate this familial transmission, and especially the role of plasma anti-HHV-8 antibody titers, we conducted a large survey in a village from Cameroon, Central Africa, including 92 families (608 individuals). Plasma samples were tested for specific IgG directed against HHV-8 lytic antigens by immunofluorescence assay, and titers were determined by 2-fold dilutions. Global HHV-8 seroprevalence was 60%, raising from 32% under 9 years up to a plateau of around 62% between 15 and 40 years. The familial correlation patterns in HHV-8 seropositive/seronegative status showed strong dependence from mother to child and between siblings. In contrast, no familial correlation in anti-HHV-8 antibody levels was observed among infected subjects. In particular, no relationship was observed between the anti-HHV-8 antibody titer of HHV-8 seropositive mothers and the proportion of their HHV-8 seropositive children. Furthermore, a random permutation study of the anti-HHV-8 antibody titers among HHV-8 infected subjects showed that the main risk factor for infection was the HHV-8 serologic status and not the antibody level. In addition, no correlation was found between anti-HHV-8 antibody levels and buffy coat HHV-8 viral loads in a subsample of 95 infected subjects. Overall, these results strongly suggest that, in this highly endemic population from Central Africa, HHV-8 transmission mainly occurs from mother to child and between siblings, and it is independent of plasma antibody levels of HHV-8 infected relatives.

Evidence for a recessive major gene predisposing to human herpesvirus 8 (HHV-8) infection in a population in which HHV-8 is endemic.

Infection by human herpesvirus 8 (HHV-8), as measured by the presence of specific antibodies, was shown in countries in which HHV-8 infection is endemic to exhibit familial aggregation and a peculiar variation with age (rapid increase until puberty followed by a plateau in young adults). To investigate whether host genetic factors could explain these findings, a segregation analysis was performed of 81 families of African origin (1623 subjects; HHV-8 seroprevalence, 11.9%) living in a village in French Guiana in which HHV-8 infection is endemic. Results provide evidence for a recessive gene controlling susceptibility or resistance to HHV-8 infection. This gene is predicted to have a major effect during childhood, with almost all homozygous predisposed subjects ( approximately 6% of the population) being infected by age 15. For nonpredisposed subjects, HHV-8 infection in childhood strongly depends on virus exposure (through an HHV-8-infected mother), whereas the risk of infection appears to be low in young adults, with no evidence for heterosexual transmission.

High titers of anti-human herpesvirus 8 antibodies in elderly males in an endemic population.

Human herpesvirus 8 (HHV8) is the etiologic agent of Kaposi's sarcoma (KS), a tumor occurring mainly among elderly men in its endemic and classical forms. The male-to-female ratio of KS in different endemic populations ranges from 3 : 1 to 15 : 1. We investigated the influence of age and gender on anti-HHV8 antibody titers among HHV8-seropositive subjects of an endemic population (1819 villagers with 874 men and 945 women) of African origin living in French Guiana. By using a specific immunofluorescence assay, we found that the overall HHV8 seroprevalence of antibodies against lytic antigens was 11.8%. There was no difference between seroprevalence in males (11.7%) and females (11.8%). Among the 214 HHV8-seropositive subjects, anti-HHV8 antibody titers were found to increase with age (P<.001) and were higher in males than in females (P =.003). The geometric mean of HHV8 antibody titers was 1 : 105 (95% confidence interval [CI] = 1 : 77 to 1 : 144) for males versus 1 : 62 (95% CI = 1 : 47 to 1 : 81) for females. The titers increased from 1 : 59 (95% CI = 1 : 43 to 1 : 80) in males younger than 40 years to 1 : 452 (95% CI = 1 : 244 to 1 : 839) in the oldest male group (aged 50 years and older). Such high antibody titers directed against lytic antigens in males aged 40 years and older parallel the increase of endemic KS incidence in older African men. Our results suggest that the role of gender should also be considered in evaluating the association between anti-HHV8 antibody titers in people aged 40 years and older and the risk of developing KS.