Genetic diversity of human immunodeficiency virus type 1 strains in Kinshasa, Zaire.

The envelope (env) gene of human immunodeficiency virus type 1 (HIV-1) was amplified by polymerase chain reaction (PCR) from the peripheral blood mononuclear cells (PBMCs) of 14 HIV-1-infected women from Kinshasa, Zaire. Amplified DNA was directly sequenced with a primer specific for the HIV-1 env C2 region. The predicted amino acid sequences for the C2-V3 region for the 14 specimens are presented. The tetrapeptide sequence, GPGQ, located at the crown of the V3 loop, is conserved in all specimens. The same tetrapeptide sequence is present in the Zairian isolate MAL, but not in other published Zairian isolates (Z6, ELI, Z321, JY1, and NDK). Sequence comparison of the env C2-V3 region among the 14 specimens from Kinshasa revealed a 9-25% range of nucleotide divergence, with an average of 16%. Divergence between the 14 specimens and the Zairian isolates MAL, Z6, ELI, Z321, JY1, and NDK ranged from 13 to 31%. A range of 18-28% nucleotide sequence divergence was demonstrated between the 14 Kinshasa specimens and the North American isolate MN. These results demonstrate the importance of examining HIV-1 samples from diverse geographic origins in the development of effective HIV-1 vaccines.

Intravenous quinine therapy of hospitalized children with Plasmodium falciparum malaria in Kinshasa, Zaire.

To examine the clinical and parasitologic efficacy of quinine, we studied 34 children (7 months-13 years old) with severe or moderately severe Plasmodium falciparum infections. Quinine 10 mg/kg every 8 hr for 3 days was administered, initially by intravenous infusion of quinine formate followed by oral quinine dihydrochloride when tolerated. Thirty-three of the 34 patients were clinically well and had negative malaria smears 7 days after the initiation of therapy; 1 child, who presented in coma, died 29 hr after enrollment. The mean fever clearance time was 44.1 hr, and the mean parasite clearance time was 59.6 hr. A mean peak quinine level of 9.7 ppm was attained after the second dose of quinine, and the minimum concentration was maintained at 5-7 ppm during the 2nd and 3rd hospital days. In vitro testing was conducted with parasites from 10 patients: 9 isolates were resistant to chloroquine, and inhibition of schizont development with quinine occurred at a concentration of 8-32 pmol/well.

Plasmodium Falciparum malaria and perinatally acquired human immunodeficiency virus type 1 infection in Kinshasa, Zaire. A prospective, longitudinal cohort study of 587 children.

BACKGROUND: It is uncertain whether Plasmodium falciparum malaria is more frequent or more severe in children with perinatally acquired human immunodeficiency virus type 1 (HIV-1) infection and whether P. falciparum infection accelerates the progression of HIV-related disease. METHODS: We conducted a prospective, longitudinal cohort study in Kinshasa, Zaire. Two hundred sixty children 5 to 9 months of age who had been born to HIV-1-seropositive mothers and 327 children of the same age who had been born to seronegative mothers were monitored intensively for malaria over a 13-month period. All episodes of fever were evaluated with blood smears for malaria, and children found to be infected with P. falciparum were treated with a standard regimen of oral quinine. RESULTS: A total of 2899 fevers were evaluated, with 271 cases of malaria identified. No statistically significant differences were found in the incidence, severity, or response to therapy of malaria among four well-defined groups of children: those with the acquired immunodeficiency syndrome (AIDS), those who were HIV-1-seropositive throughout the study, those who were born to HIV-1-seropositive mothers but reverted to seronegative, and those who were seronegative throughout the study. During the 13-month period the incidence of malaria in the 36 children with HIV infection in whom AIDS developed was lower, although not significantly so, than in the 37 in whom AIDS did not. CONCLUSIONS: In this study malaria was not more frequent or more severe in children with progressive HIV-1 infection and malaria did not appear to accelerate the rate of progression of HIV-1 disease.