Acquired Immunodeficiency Syndrome: Adu-Sarkodie Y

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A digest of articles written 1999 and later, on the topic "Acquired Immunodeficiency Syndrome," originating from Planet Earth —» Adu-Sarkodie Y.  Display:  All Citations ·  All Abstracts
1 Article AIDS in an HIV-seronegative Ghanaian woman with intersubtype A/G recombinant HIV-1 infection. 2000

Candotti D, Adu-Sarkodie Y, Davies F, Baldrich-Rubio E, Stirrups K, Lee H, Allain JP. · Department of Haematology, University of Cambridge, United Kingdom. · J Med Virol. · Pubmed #10935981 No free full text.

Abstract: A 29-year-old Ghanaian woman who developed AIDS while being HIV-antibody seronegative was investigated during a collaborative study aimed at the identification of viral causes of a HIV-seronegative AIDS syndrome in West Africa. Plasma was screened with a panel of EIA tests for antibodies to HIV and HIV-1 p24 antigen. Retroviral infection was investigated by detection of reverse transcriptase (RT) activity in plasma, viral RNA amplification and quantification, and virus isolation. Positive amplification products were sequenced and phylogenetic analyses were carried out. Most EIA tests were unable to demonstrate the presence of anti-HIV anti-bodies, whereas confirmatory assays yielded inconclusive results. Retroviral infection was documented by detection of RT activity, HIV-1-specific genomic amplification and virus isolation. This virus was HIV-1 subtype A with an unusual six amino acid insertion in the gp120 V4 loop and with the nef gene of subtype G. The patient's plasma did not react with either autologous or heterologous viral lysates or HIV-1 peptides, whereas antibodies to other viral antigens were present. In conclusion, the Ghanaian patient exhibited a rare subtype A/G recombinant HIV-1 infection with a near absence of a HIV-specific humoral response. The lack of detectable antibody response might be due to either a highly pathogenic, rapidly fatal, HIV-1 infection preventing the development of the typical humoral immune response or to a host-related dysfunction of the immune system. Direct antigenemia or genomic detection of the virus should be undertaken when clinical or biological data suggests an HIV infection in the absence of serological evidence.

2 Article Relationship between immunoclinical status and prevalence of viral sexually transmitted diseases among human immunodeficiency virus-1 seropositive patients in Ghana. 1999

Brandful JA, Apeagyei FA, Ampofo WK, Adu-Sarkodie Y, Ansah JE, Nuvor V, Aidoo S, Ishikawa K, Sata T, Yamamoto N, Yamazaki S. · Virology Unit, Noguchi Memorial Institute for Medical Research (NMIMR), University of Ghana, Legon. · Viral Immunol. · Pubmed #10413359 No free full text.

Abstract: In view of the strong association between the acquired immunodeficiency syndrome (AIDS) and sexually transmitted diseases (STDs), we screened 182 human immunodeficiency virus (HIV)-1 infected patients over a 15-month period for serological markers to previously encountered or current STDs, most of viral etiology. The relationship between their immunological and clinical status and the prevalence of STDs was assessed and compared with that of 88 HIV-seronegative patients. Hepatitis B virus and Treponema pallidum were the most frequently occurring pathogens in both HIV-1-infected and HIV-seronegative patients. Hepatitis C virus (HCV) infection was also observed in both groups, but no HIV-seronegative patient was infected with human T-lymphotropic virus type 1 (HTLV-1). The Centers for Disease Control clinical staging of A1 through C3, representing asymptomatic to severe AIDS conditions, was observed in HIV-1 patients with or without STDs. A mean CD4 count of 288 cells per microliter (95% CI of 237-340 cells per microliter) in HIV-1 patients was significantly lower (P < 0.05) than that in HIV-seronegative individuals with 1019 cells per microliter (95% CI of 924-1115 cells per microliter), irrespective of whether subjects in either group had previous or current STDs. The mean CD4 count of patients with a single infection from HIV-1 was not significantly different (P = 0.36) from that of HIV-1 patients with multiple infections. HIV-1 infection alone appears to be responsible for the marked immunodeficiency status of seropositive patients observed in this study.