Women with genital schistosomiasis had an almost three-fold risk of having HIV in this rural Zimbabwean community. Prospective studies are needed to confirm the association.

Up to 75% of women with urinary schistosomiasis have Schistosoma haematobium ova in the genitals. This study aimed to describe the prevalence of gynecologic S. haematobium infection and to differentiate the disease from sexually transmitted infections (STIs). Gynecologic and laboratory investigations for S. haematobium and STIs were performed in 527 women between the ages of 20 and 49 in rural Zimbabwe. Genital homogenous yellow and/or grainy sandy patches, the commonest type of genital pathology, were identified in 243 (46%) women. Grainy sandy patches were significantly associated with S. haematobium ova only. Genital S. haematobium ova was also significantly associated with homogenous yellow sandy patches, mucosal bleeding, and abnormal blood vessels. The presence of ova was not a predictor for ulcers, papillomata, leukoplakia, polyps, or cell atypia. Mucosal sandy patches seem to be pathognomonic for S. haematobium infection in the female genitals. Coexistence of ova and other lesions may not be causal.

To determine whether treatment of schistosomiasis has an effect on the course of human immunodeficienc virus type 1 (HIV-1) infection, individuals with schistosomiasis and with or without HIV-1 infection were randomized to receive praziquantel treatment at inclusion or after a delay of 3 months; 287 participants were included in the study, and 227 (79%) were followed up. Among the 130 participants who were coinfected, those who received early treatment ( ) had a n p 64 significantl lower increase in plasma HIV-1 RNA load than did those who received delayed treatment ( ) ( ); n p 66 P ! .05 this difference was associated with no change in plasma HIV-1 RNA load in the early intervention group ( ) and an P p .99 increase in plasma HIV-1 RNA load in the delayed intervention group ( ). Among the 227 participants who were fol-P ! .01 lowed up, those who received early treatment ( ) had n p 105 an increase in CD4 cell count, whereas those who received delayed treatment ( ) did not ( ); this effect did n p 122 P ! .05 not differ between participants when stratifie by HIV-1 infection status (). The present study suggests that treat-P p .17 ment of schistosomiasis can reduce the rate of viral replication and increase CD4 cell count in the coinfected host.Immune activation caused by a higher prevalence of concurrent infections has been hypothesized to be a driving factor for in-

Background To date little has been published about epidemiology and public health capacity (training, research, funding, human resources) in WHO/AFRO to help guide future planning by various stakeholders.Methods A bibliometric analysis was performed to identify published epidemiological research. Information about epidemiology and public health training, current research and challenges was collected from key informants using a standardized questionnaire.Results From 1991 to 2010, epidemiology and public health research output in the WHO/AFRO region increased from 172 to 1086 peer-reviewed articles per annum [annual percentage change (APC) = 10.1%, P for trend < 0.001]. The most common topics were HIV/AIDS (11.3%), malaria (8.6%) and tuberculosis (7.1%). Similarly, numbers of first authors (APC = 7.3%, P for trend < 0.001), corresponding authors (APC = 8.4%, P for trend < 0.001) and last authors (APC = 8.5%, P for trend < 0.001) from Africa increased during the same period. However, an overwhelming majority of respondents (>90%) reported that this increase is only rarely linked to regional post-graduate training programmes in epidemiology. South Africa leads in publications (1978/8835, 22.4%), followed by Kenya (851/8835, 9.6%), Nigeria (758/8835, 8.6%), Tanzania (549/8835, 6.2%) and Uganda (428/8835, 4.8%) (P < 0.001, each vs South Africa). Independent predictors of relevant research productivity were ‘in-country numbers of epidemiology or public health programmes’ [incidence rate ratio (IRR) = 3.41; 95% confidence interval (CI) 1.90–6.11; P = 0.03] and ‘number of HIV/AIDS patients’ (IRR = 1.30; 95% CI 1.02–1.66; P < 0.001).Conclusions Since 1991, there has been increasing epidemiological research productivity in WHO/AFRO that is associated with the number of epidemiology programmes and burden of HIV/AIDS cases. More capacity building and training initiatives in epidemiology are required to promote research and address the public health challenges facing the continent.

The present study suggests that adult HIV-1-related immunodeficiency does not impair the ability to excrete eggs in low-intensity infection with S. haematobium, S. mansoni, or both and that infection with HIV-1 may not have major implications for diagnosis and surveillance of schistosomiasis.

HIV-1 subtype C (C-HIV) is responsible for most HIV-1 cases worldwide. Although the pathogenesis of C-HIV is thought to predominantly involve CCR5-restricted (R5) strains, we do not have a firm understanding of how frequently CXCR4-using (X4 and R5X4) variants emerge in subjects with progressive C-HIV infection. Nor do we completely understand the molecular determinants of coreceptor switching by C-HIV variants. Here, we characterized a panel of HIV-1 envelope glycoproteins (Envs) (n = 300) cloned sequentially from plasma of 21 antiretroviral therapy (ART)-naïve subjects who experienced progression from chronic to advanced stages of C-HIV infection, and show that CXCR4-using C-HIV variants emerged in only one individual. Mutagenesis studies and structural models suggest that the evolution of R5 to X4 variants in this subject principally involved acquisition of an “Ile-Gly” insertion in the gp120 V3 loop and replacement of the V3 “Gly-Pro-Gly” crown with a “Gly-Arg-Gly” motif, but that the accumulation of additional gp120 “scaffold” mutations was required for these V3 loop changes to confer functional effects. In this context, either of the V3 loop changes could confer possible transitional R5X4 phenotypes, but when present together they completely abolished CCR5 usage and conferred the X4 phenotype. Our results show that the emergence of CXCR4-using strains is rare in this cohort of untreated individuals with advanced C-HIV infection. In the subject where X4 variants did emerge, alterations in the gp120 V3 loop were necessary but not sufficient to confer CXCR4 usage.

Genital schistosomiasis may be a differential diagnosis to the STDs in women who have been exposed to fresh water in endemic areas. Because of the chronic nature of the disease in adults, we suggest to pay special attention to the prevention of morbidity.

Cervical cancer is a leading cause of cancer-related deaths in developing countries, and the human papillomavirus (HPV) is linked etiologically to cervical cancer. Hence, a vaccine which prevents HPV-associated cervical cancer would have the most impact in developing countries, including the African continent. The type-specific immune response towards HPV virus-like particles, in combination with geographical variation in the prevalence of HPV, necessitates the presence of multiple HPV type antigens in a single vaccine cocktail in order to provide relevant protection. We aimed to investigate whether co-infection with HIV, which is highly prevalent in Africa, plays a role in HPV genotype distribution. After informed consent, HPV detection by GP5+/6+ PCR and HIV detection by serology was carried out on 236 women from the rural north-western part of Zimbabwe. The prevalence of HPV was higher in HIV positive women (54%) than in HIV negative women (27%). Certain HPV types (HPV types 11, 39, 43, 51, and 59, P-values ranging from 0.017 to 0.067) occurred more frequently in HIV positive women. Only high-risk HPV, and not HIV, was associated significantly with cervical intraepithelial neoplasia in multiple regression analysis. In conclusion, a high prevalence of HPV was found in a rural community, where regular Papanicolaou (Pap) smears would be a logistic and economic impossibility, but where free vaccination programmes against other infections are already established. The results suggest that HIV co-infection may have an impact on HPV genotype distribution.