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9 oct. 2008

Mutations in PFCRT K76T do not correlate with sulfadoxine-pyrimethamine-amodiaquine failure in Pikine, Senegal.

Sarr O, Ahouidi AD, Ly O, Daily JP, Ndiaye D, Ndir O, Mboup S, Wirth DF.

Mutations in PFCRT K76T do not correlate with sulfadoxine-pyrimethamine-amodiaquine failure in Pikine, Senegal.

Parasitol Res. 2008 Sep;103(4):765-9. Epub 2008 Jun 5.
PMID: 18523801 [PubMed - indexed for MEDLINE]

Laboratory of Bacteriology and Virology, Hopital Aristide Le Dantec, BP 7325, Dakar, Senegal. osarr@hsph.harvard.edu.

In 2003, the high level of chloroquine (CQ) treatment failure for uncomplicated Plasmodium falciparum malaria cases has led Senegal to adopt a new combination therapy with sulfadoxine-pyrimethamine and amodiaquine (SP-AQ). From September through November 2004, we used the 14-day World Health Organization follow-up protocol to assess the therapeutic response in patients with uncomplicated P. falciparum malaria in an area of high prevalence of pfcrt T76 mutant allele and SP resistance mutations. Of the 82 patients who were recruited, 68 (82.9%) completed follow-up. The response of the patients to treatment was adequate clinical response for 63 out of 68 patients (92.6%), while five (7.4%) clinical failures were recorded, four early treatment failures, and one late treatment failure. The prevalence of the pfcrt T76 allele at day 0 was 59.5%. The two-sided Fisher's exact test did not show an association between pfcrt T76 allele and treatment failure (p=0.167). The transitory treatment is effective and safe. However, the presence of high levels of mutant alleles points out the need to closely monitor the new therapeutic regimen.

Source

Higher homologous and lower cross-reactive Gag-specific T-cell responses in human immunodeficiency virus type 2 (HIV-2) than in HIV-1 infection.

J Virol. 2008 Sep;82(17):8619-28. Epub 2008 Jun 18.Click here to read Links
Higher homologous and lower cross-reactive Gag-specific T-cell responses in human immunodeficiency virus type 2 (HIV-2) than in HIV-1 infection.
Jennes W, Camara M, Dièye T, Mboup S, Kestens L.

Department of Microbiology, Laboratory of Immunology, Institute of Tropical Medicine, Antwerp, Belgium. wjennes@itg.be

Human immunodeficiency virus type 2 (HIV-2) infection results in slower CD4(+) T-cell decline, lower plasma viral load levels, and hence slower progression of the disease than does HIV-1 infection. Although the reasons for this are not clear, it is possible that HIV-2 replication is more effectively controlled by host responses. We used aligned pools of overlapping HIV-1 and HIV-2 Gag peptides in an enhanced gamma interferon enzyme-linked immunospot assay to compare the levels of homologous and cross-reactive Gag-specific T-cell responses between HIV-1- and HIV-2-infected patients. HIV-2-infected patients showed broader and stronger homologous Gag-specific T-cell responses than HIV-1-infected patients. In contrast, the cross-reactive T-cell responses in HIV-2-infected patients were both narrower and weaker than those in HIV-1-infected patients, in line with overall weaker correlations between homologous and heterologous T-cell responses among HIV-2-infected patients than among HIV-1-infected patients. Cross-reactive responses in HIV-2-infected patients tended to correlate directly with HIV-1/HIV-2 Gag sequence similarities; this was not found in HIV-1-infected patients. The CD4(+) T-cell counts of HIV-2-infected patients correlated directly with homologous responses and inversely with cross-reactive responses; this was not found in HIV-1-infected patients. Our data support a model whereby high-level HIV-2-specific T-cell responses control the replication of HIV-2, thus limiting viral diversification and priming of HIV-1 cross-reactive T-cell responses over time. However, we cannot exclude the possibility that HIV-2 replication is controlled by other host factors and that HIV-2-specific T-cell responses are better maintained in the context of slow viral divergence and a less damaged immune system. Understanding the nature of immune control of HIV-2 infection could be crucial for HIV vaccine design.

http://www.ncbi.nlm.nih.gov/pubmed/18562522?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum