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Background: In sub-Saharan Africa, co-infection with HIV and malaria is probably very common. Although an interaction between the two infections is biologically plausible, it has not been investigated thoroughly. Objectives: To evaluate the association firstly between co-infection with HIV and malaria parasites and the occurrence of acute fever, and secondly between HIV infection and clinical malaria, defined as the presence of acute fever and malaria parasites. Methods: A hospital-based case‐control study was conducted in Gulu District (northern Uganda), an area endemic for malaria and with a high HIV prevalence. HIV testing and malaria parasite quantification were performed on 167 consecutive adult outpatients with acute fever and no signs or symptoms of localized infection, and on 134 consecutive adult in-patients without fever who were admitted for non-HIV-related trauma or elective surgery. Results: No significant association with acute fever was observed for single infection with either malaria parasites [adjusted odds ratio (AOR), 1.75; 95% confidence interval (CI), 0.73‐4.21] or HIV (AOR, 1.01; 95% CI, 0.51‐2.03), whereas a significant association was observed for co-infection (AOR, 9.75; 95% CI, 1.19‐80.00). An association was found between HIV infection and clinical malaria (AOR, 2.34; 95% CI, 0.89‐6.17); the association became statistically significant when the definition of clinical malaria included a cut-off for parasite density (50 th percentile; i.e., 586 parasites/Il; AOR, 3.61; 95% CI, 1.04‐12.52). Conclusions: Despite the limited statistical power, the results of our study show an association between HIV infection and clinical malaria; if confirmed, this finding could be important for public health in sub-Saharan Africa.

Background: HIV infection in Africa is associated with immune activation and a cytokine profile that stimulates CCR5 expression. We investigated whether this immune activation is environmentally driven; if a dominant expression of CCR5 could indeed be detected in African individuals; and if R5 HIV strains would be prevalent in this population. Methods: Freshly drawn peripheral blood mononuclear cells from HIV-uninfected African and Italian individuals living in rural Africa, from HIV-uninfected Africans and Italians living in Italy, and from HIV-infected African and Italian patients were analysed. Determinations of HIV coreceptor-specific mRNAs and immunophenotype analyses were performed in all samples. Virological analyses included virus isolation and characterization of plasma neutralizing activity. Findings: Results showed that: immune activation is detected both in Italian and African HIV-uninfected individuals living in Africa but not in African subjects living in Italy; CCR5-specific mRNA is augmented and the surface expression of CCR5 is increased in African compared with Italian residents (CXCR4-specific mRNA is comparable); R5-HIV strains are isolated prevalently from lymphocytes of African HIVinfected patients; and plasma neutralizing activity in HIV-infected African patients is mostly specific for R5 strains. Conclusions: Immune activation in African residents is environmentally driven and not genetically predetermined. This immune activation results in a skewing of the CCR5 : CXCR4 ratio which is associated with a prevalent isolation of R5 viruses. These data suggest that the selection of the predominant virus strain within the population could be influenced by an immunologically driven pattern of HIV co receptor expression.

The concentration of type 1 and type 2 cytokines and fibroblast-associated apoptosis-1 soluble receptor (sAPO-1/Fas) was analysed in the sera of Ugandan and Italian HIV-1-seropositive and seronegative individuals. The data were compared to determine whether the immunological status of these groups was different.Sixty-seven Ugandan and 30 Italian HIV-positive patients were analysed and stratified according to CD4 counts (group 1,500 x 10(6)/l; group 2, 200-500 x 10(6)/l; group 3,200 x 10(6)/l). Sera from 15 Ugandan and 11 Italian HIV-negative blood donors were also analysed. Serum concentration of type 1 cytokines [interleukin (IL)-2, IL-12, and interferon (IFN)-gamma] and type 2 cytokines (IL-4 and IL-10), and sAPO-1/Fas were measured by enzyme-linked immunosorbent assay.Serum levels of IL-2, IFN-gamma and IL-10 but not of IL-4 and IL-12, were elevated in HIV-positive group 1 and 2 Africans compared with HIV-positive Italian individuals. IL-4 was mildly augmented in HIV-positive group 3 African patients. Serum concentration of sAPO-1/Fas was reduced in HIV-positive Africans compared with HIV-positive Italian individuals. Finally, serum levels of IL-2 and IL-10 were increased and sAPO-1/Fas reduced when sera of HIV-negative African healthy controls were compared with their Italian counterparts. The ratio of type 1/type 2 cytokines was roughly 1.0 in HIV-negative African controls, and much greater than 1.0 in HIV-negative Italian controls.These preliminary findings indicate that immune activation is present in African HIV infection. Furthermore, these data raise the possibility that abnormal immune activation and increased susceptibility to antigen-induced cell death is present even in HIV-negative African controls.

Although Ebola virus (EBOV) is transmitted by unprotected physical contact with infected persons, few data exist on which specific bodily fluids are infected or on the risk of fomite transmission. Therefore, we tested various clinical specimens from 26 laboratory-confirmed cases of Ebola hemorrhagic fever, as well as environmental specimens collected from an isolation ward, for the presence of EBOV. Virus was detected by culture and/or reverse-transcription polymerase chain reaction in 16 of 54 clinical specimens (including saliva, stool, semen, breast milk, tears, nasal blood, and a skin swab) and in 2 of 33 environmental specimens. We conclude that EBOV is shed in a wide variety of bodily fluids during the acute period of illness but that the risk of transmission from fomites in an isolation ward and from convalescent patients is low when currently recommended infection control guidelines for the viral hemorrhagic fevers are followed.

The objective was to estimate HIV-1 prevalence among women attending an antenatal clinic in the Gulu District (North Uganda) and based on these data among the districts female population. Anonymous HIV-1 screening was performed for 8555 antenatal clinic attendees aged 15-39 years in the period 1993-97. The results were used to estimate the prevalence among the districts female population accounting for differences in fertility rates by HIV-1 serostatus. Among antenatal clinic attendees HIV-1 prevalence showed a significant linear decrease (P < 0.001) from 26.0% in 1993 [95% confidence interval (CI) 23.2-29.0%] to 16.1% in 1997 (95% CI 14.8-17.5%). This decrease was mostly due to a marked decrease until 1995 (14.3%; 95% CI 12.7-16.0%) and was more pronounced among women aged under 30 years (P < 0.001) from both urban and rural areas (P < 0.001). The risk of being infected was higher among women from urban areas (Gulu Municipality) both over the entire period (adjusted prevalence proportion ratio = 1.54; 95% CI 1.40-1.68) and by individual year. The estimated prevalence for the 15-39 year old female population standardized by age and area of residence decreased from 25.4% in 1993-94 to 17.8% in 1996-97; these rates were 1.22 and 1.28 times higher respectively than those among antenatal clinic attendees. The trend of decrease among young women for whom changes in HIV-1 prevalence more closely reflect incidence could be partially due to a reduction in risk behavior and a consequent decreasing incidence. Differences in fertility rates by HIV-1 serostatus should be addressed when using antenatal clinic data to estimate prevalence among the general female population. (authors)

From January 1989 to April 1996 15568 individuals (5057 inpatients 3466 outpatients 5438 women attending the antenatal clinic and 1607 secondary students) were screened for HIV-1 virus at St. Marys Lacor Hospital northern Ugandas main hospital. For inpatients estimated prevalence rates with exact binomial 95% confidence intervals were 57.9 (53.3-62.4) for 1989 52.1 (49.0-55.1) for 1990 51.9 (48.1-55.6) for 1991 64.2 (60.2-68.2) for 1992 56.0 (51.7-60.1) for 1993 65.4 (62.3-68.5) for 1994 57.2 (52.6-61.8) for 1995 and 56.1 (50.0-62.1) for 1996. For outpatients they were 44.5 (38.8-50.2) for 1989 53.3 (49.6-56.9) for 1990 60.1 (51.6-8.2) for 1991 64.1 (55.3-72.3) for 1992 45.8 (39.1-52.7) for 1993 44.1 (40.1-47.6) for 1994 39.3 (36.0-42.8) for 1995 and 43.7 (38.0-49.6) for 1996. For pregnant women they were 27.1 (24.4-30.0) for 1993 21.9 (20.2-23.8) for 1994 14.7 (13.1-16.4) for 1995 and 11.7 (8.8-15.1) for 1996. For secondary school students they were 2.0 (1.1-3.3) for 1994 1.4 (0.7-2.5) for 1995 and 1.8 (0.4-5.1) for 1996. Adjusted odds ratios (ORs) were calculated using a logistic regression model that controlled for gender group and year tested. Logistic regression models were also used to test for each group the presence of a significant linear change over time in risk of being infected controlling for gender. The adjusted OR per group with a 95% confidence interval for inpatients was 79.1 (53.6-116.6); for outpatients it was 68.4 (46.3-101.1); for pregnant women it was 14.3 (9.7-21.1); and for secondary school students it was 1.0. 48.4 % of students were not yet sexually active. The adjusted OR with a 95% confidence interval/year tested was 1.1 (0.9-.4) for 1989 1.1 (1.0-1.4) for 1990 1.1 (0.9-1.4) for 1991 1.8 (1.5-2.2) for 1992 1.6 (1.3-1.9) for 1993 1.7 (1.4-2.0) for 1994 1.0 (0.9-1.2) for 1995 and 1.0 for 1996. A significant decrease was found for pregnant women (OR = 0.69; p < .001). Stable or decreasing HIV-1 seroprevalence over time does not necessarily imply decreasing incidence; increasing mortality and migration among HIV-1 infected persons can obscure increasing incidence. The data indicate a homogeneity in the epidemic throughout Uganda.

Immune activation induced by chronic infections dietary limitations and poor hygienic conditions is thought to be present in African HIV infection and is at the heart of the hypothesis that HIV in Africa could be highly associated with immunopathogenetic mechanisms. Immunological and virological parameters were analyzed in fresh peripheral blood mononuclear cells (PBMCs) of 43 Ugandan and 33 Italian HIV-infected patients with advanced HIV disease and comparable CD4 and CD8 counts sex and age. Functional and phenotypic analyses were performed. Results were then compared with those of 18 Ugandan and 18 Italian age- and sex-matched HIV-seronegative controls. HIV plasma viremia was analyzed by competitive polymerase chain reaction (PCR) and branched DNA techniques. Study results confirm that immune activation accompanies HIV infection in Africa and is present even in HIV-seronegative healthy controls. Immune activation increases in-vitro susceptibility of peripheral lymphocytes to HIV infection.