SidaSubSaharaV1, Istex, Corpus, bibRecord, 003D07

AIDS in an HIV‐seronegative Ghanaian woman with intersubtype A/G recombinant HIV‐1 infection

Identifieur interne : 003D07 ( Istex/Corpus ); précédent : 003D06; suivant : 003D08

AIDS in an HIV‐seronegative Ghanaian woman with intersubtype A/G recombinant HIV‐1 infection

Auteurs : Daniel Candotti ; Yaw Adu-Sarkodie ; Fiona Davies ; Eva Baldrich-Rubio ; Kathleen Stirrups ; Helen Lee ; Jean-Pierre Allain

Source :

Journal of Medical Virology [ 0146-6615 ] ; 2000-09.

RBID : ISTEX:BAB7189089E6E0449BC45B882663FA86FC0801FE

English descriptors

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. J. Med. Virol. 62:1–8, 2000. © 2000 Wiley‐Liss, Inc.

Url:

https://api.istex.fr/document/BAB7189089E6E0449BC45B882663FA86FC0801FE/fulltext/pdf

DOI: 10.1002/1096-9071(200009)62:1<1::AID-JMV1>3.0.CO;2-3

Links to Exploration step

ISTEX:BAB7189089E6E0449BC45B882663FA86FC0801FE

Le document en format XML

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<front><div type="abstract" xml:lang="en">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. J. Med. Virol. 62:1–8, 2000. © 2000 Wiley‐Liss, Inc.</div>
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<p>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 <hi rend="italic">nef</hi>
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<abstract lang="en">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. J. Med. Virol. 62:1–8, 2000. © 2000 Wiley‐Liss, Inc.</abstract>
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	Le SIDA en Afrique subsaharienne (serveur d'exploration)
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Le SIDA en Afrique subsaharienne (serveur d'exploration)

AIDS in an HIV‐seronegative Ghanaian woman with intersubtype A/G recombinant HIV‐1 infection

AIDS in an HIV‐seronegative Ghanaian woman with intersubtype A/G recombinant HIV‐1 infection

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