People living with HIV co‐infected with the Kaposi Sarcoma‐associated Herpes Virus have a distinct HIV Tat profile and higher rates of antiretroviral virologic failure, more evident among those with Kaposi's sarcoma
Kaposi sarcoma (KS) is a neoplasm of vascular origin that promotes angiogenesis and the growth of endothelial cells triggered by the Kaposi Sarcoma‐associated Herpes Virus (KSHV). When associated with HIV, KSHV becomes more aggressive and rapidly evolves. The HIV‐1 TAT protein can be essential in de...
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| creator | Suterio, Dalila G. Hunter, James R. Tenore, Simone B. Pimentel, Sidnei R. Galinskas, Juliana Dias, Danilo A. Bellini, Débora C. Ferreira, Paulo A. Diaz, Ricardo Sobhie |
| description | Kaposi sarcoma (KS) is a neoplasm of vascular origin that promotes angiogenesis and the growth of endothelial cells triggered by the Kaposi Sarcoma‐associated Herpes Virus (KSHV). When associated with HIV, KSHV becomes more aggressive and rapidly evolves. The HIV‐1 TAT protein can be essential in developing AIDS‐associated KS by promoting angiogenesis and increasing KSHV replication. Therefore, we evaluated the genetic profile of the first exon of tat gene among groups of people living with HIV (PLHIV) with (case group, n = 36) or without KS, this later with (positive control group, n = 46) and without KSHV infection (negative control group, n = 24); all individuals under antiretroviral therapy. The genetic diversity, the DN/DS ratio, and the genetic entropy of the first exon of tat were higher in the case group, followed by the positive control group, which was higher than the negative control group. The number of tat codons under positive selection was seven in the case group, six in the positive control group, and one in the negative control group. The prevalence of HIV viral loads below the detection limit was equal in the case and positive control groups, which were lower than in the negative control group. The mean CD4+ T cell counts were higher in the negative control group, followed by the positive control group, and followed by the case group. These results emphasize the negative influence of KSHV in antiretroviral treatment, as well as the HIV‐specific TAT profile among PLHIV who developed KS. |
| doi_str_mv | 10.1002/jmv.29840 |
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When associated with HIV, KSHV becomes more aggressive and rapidly evolves. The HIV‐1 TAT protein can be essential in developing AIDS‐associated KS by promoting angiogenesis and increasing KSHV replication. Therefore, we evaluated the genetic profile of the first exon of tat gene among groups of people living with HIV (PLHIV) with (case group, n = 36) or without KS, this later with (positive control group, n = 46) and without KSHV infection (negative control group, n = 24); all individuals under antiretroviral therapy. The genetic diversity, the DN/DS ratio, and the genetic entropy of the first exon of tat were higher in the case group, followed by the positive control group, which was higher than the negative control group. The number of tat codons under positive selection was seven in the case group, six in the positive control group, and one in the negative control group. The prevalence of HIV viral loads below the detection limit was equal in the case and positive control groups, which were lower than in the negative control group. The mean CD4+ T cell counts were higher in the negative control group, followed by the positive control group, and followed by the case group. These results emphasize the negative influence of KSHV in antiretroviral treatment, as well as the HIV‐specific TAT profile among PLHIV who developed KS.</description><identifier>ISSN: 0146-6615</identifier><identifier>ISSN: 1096-9071</identifier><identifier>EISSN: 1096-9071</identifier><identifier>DOI: 10.1002/jmv.29840</identifier><identifier>PMID: 39092805</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adult ; Angiogenesis ; Anti-Retroviral Agents - therapeutic use ; Antiretroviral agents ; Antiretroviral drugs ; Antiretroviral therapy ; CD4 antigen ; CD4 Lymphocyte Count ; Clonal selection ; Codons ; Coinfection - drug therapy ; Coinfection - virology ; Endothelial cells ; Female ; Genetic diversity ; Genetic Variation ; Herpes viruses ; Herpesvirus 8, Human - genetics ; HIV ; HIV Infections - complications ; HIV Infections - drug therapy ; HIV Infections - virology ; HIV-1 - drug effects ; HIV-1 - genetics ; HIV‐1 ; Human immunodeficiency virus ; Humans ; Kaposi sarcoma ; Kaposi Sarcoma‐associated Herpes Virus ; Kaposi's sarcoma ; Kaposis sarcoma ; Lymphocytes ; Lymphocytes T ; Male ; Middle Aged ; Positive selection ; Sarcoma ; Sarcoma, Kaposi - virology ; tat ; Tat gene ; tat Gene Products, Human Immunodeficiency Virus - genetics ; Tat protein ; Viral Load</subject><ispartof>Journal of medical virology, 2024-08, Vol.96 (8), p.e29840-n/a</ispartof><rights>2024 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3480-816a6959eae58be703033d080386756bef017d9a25a162ec2d6d57b69478bb523</cites><orcidid>0000-0001-9524-0629 ; 0000-0002-8395-7304</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjmv.29840$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjmv.29840$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39092805$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suterio, Dalila G.</creatorcontrib><creatorcontrib>Hunter, James R.</creatorcontrib><creatorcontrib>Tenore, Simone B.</creatorcontrib><creatorcontrib>Pimentel, Sidnei R.</creatorcontrib><creatorcontrib>Galinskas, Juliana</creatorcontrib><creatorcontrib>Dias, Danilo A.</creatorcontrib><creatorcontrib>Bellini, Débora C.</creatorcontrib><creatorcontrib>Ferreira, Paulo A.</creatorcontrib><creatorcontrib>Diaz, Ricardo Sobhie</creatorcontrib><title>People living with HIV co‐infected with the Kaposi Sarcoma‐associated Herpes Virus have a distinct HIV Tat profile and higher rates of antiretroviral virologic failure, more evident among those with Kaposi's sarcoma</title><title>Journal of medical virology</title><addtitle>J Med Virol</addtitle><description>Kaposi sarcoma (KS) is a neoplasm of vascular origin that promotes angiogenesis and the growth of endothelial cells triggered by the Kaposi Sarcoma‐associated Herpes Virus (KSHV). When associated with HIV, KSHV becomes more aggressive and rapidly evolves. The HIV‐1 TAT protein can be essential in developing AIDS‐associated KS by promoting angiogenesis and increasing KSHV replication. Therefore, we evaluated the genetic profile of the first exon of tat gene among groups of people living with HIV (PLHIV) with (case group, n = 36) or without KS, this later with (positive control group, n = 46) and without KSHV infection (negative control group, n = 24); all individuals under antiretroviral therapy. The genetic diversity, the DN/DS ratio, and the genetic entropy of the first exon of tat were higher in the case group, followed by the positive control group, which was higher than the negative control group. The number of tat codons under positive selection was seven in the case group, six in the positive control group, and one in the negative control group. The prevalence of HIV viral loads below the detection limit was equal in the case and positive control groups, which were lower than in the negative control group. The mean CD4+ T cell counts were higher in the negative control group, followed by the positive control group, and followed by the case group. These results emphasize the negative influence of KSHV in antiretroviral treatment, as well as the HIV‐specific TAT profile among PLHIV who developed KS.</description><subject>Adult</subject><subject>Angiogenesis</subject><subject>Anti-Retroviral Agents - therapeutic use</subject><subject>Antiretroviral agents</subject><subject>Antiretroviral drugs</subject><subject>Antiretroviral therapy</subject><subject>CD4 antigen</subject><subject>CD4 Lymphocyte Count</subject><subject>Clonal selection</subject><subject>Codons</subject><subject>Coinfection - drug therapy</subject><subject>Coinfection - virology</subject><subject>Endothelial cells</subject><subject>Female</subject><subject>Genetic diversity</subject><subject>Genetic Variation</subject><subject>Herpes viruses</subject><subject>Herpesvirus 8, Human - genetics</subject><subject>HIV</subject><subject>HIV Infections - complications</subject><subject>HIV Infections - drug therapy</subject><subject>HIV Infections - virology</subject><subject>HIV-1 - drug effects</subject><subject>HIV-1 - genetics</subject><subject>HIV‐1</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Kaposi sarcoma</subject><subject>Kaposi Sarcoma‐associated Herpes Virus</subject><subject>Kaposi's sarcoma</subject><subject>Kaposis sarcoma</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Positive selection</subject><subject>Sarcoma</subject><subject>Sarcoma, Kaposi - virology</subject><subject>tat</subject><subject>Tat gene</subject><subject>tat Gene Products, Human Immunodeficiency Virus - genetics</subject><subject>Tat protein</subject><subject>Viral Load</subject><issn>0146-6615</issn><issn>1096-9071</issn><issn>1096-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAURi0EokNhwQsgSywAibR2Mv5bogqYQhFIlNlGjnMz8SiJU9tJ1R2PwPt11yfBbQoLJDa2dHX8-dgfQs8pOaKE5Mf7fj7KlVyTB2hFieKZIoI-RCtC1zzjnLID9CSEPSFEqjx_jA4KRVQuCVuh62_gxg5wZ2c77PCljS3enG6xcTc_f9mhAROhXsaxBfxZjy5Y_F1743qdEB2CM1bfQhvwIwS8tX4KuNUzYI1rG6IdTLzLPNcRj941Nt2nhxq3dteCxz6dDtg1aRath-jdbL3ucFpd53bW4EbbbvLwFvfOA4bZ1jBErHuXjGPrAiyCi9yrgMOi9xQ9anQX4Nn9foh-fHh_frLJzr5-PD15d5aZYi1JJinXXDEFGpisQJCCFEVNJCkkF4xX0BAqaqVzpinPweQ1r5mouFoLWVUsLw7R6yU3Pe5ighDL3gYDXacHcFMoCyJFwZgUPKEv_0H3bvJDskuUEpxKJVSi3iyU8S4ED005ettrf1VSUt42XqbGy7vGE_viPnGqeqj_kn8qTsDxAlymf7_6f1L56ct2ifwN3Ii6PA</recordid><startdate>202408</startdate><enddate>202408</enddate><creator>Suterio, Dalila G.</creator><creator>Hunter, James R.</creator><creator>Tenore, Simone B.</creator><creator>Pimentel, Sidnei R.</creator><creator>Galinskas, Juliana</creator><creator>Dias, Danilo A.</creator><creator>Bellini, Débora C.</creator><creator>Ferreira, Paulo A.</creator><creator>Diaz, Ricardo Sobhie</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9524-0629</orcidid><orcidid>https://orcid.org/0000-0002-8395-7304</orcidid></search><sort><creationdate>202408</creationdate><title>People living with HIV co‐infected with the Kaposi Sarcoma‐associated Herpes Virus have a distinct HIV Tat profile and higher rates of antiretroviral virologic failure, more evident among those with Kaposi's sarcoma</title><author>Suterio, Dalila G. ; 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When associated with HIV, KSHV becomes more aggressive and rapidly evolves. The HIV‐1 TAT protein can be essential in developing AIDS‐associated KS by promoting angiogenesis and increasing KSHV replication. Therefore, we evaluated the genetic profile of the first exon of tat gene among groups of people living with HIV (PLHIV) with (case group, n = 36) or without KS, this later with (positive control group, n = 46) and without KSHV infection (negative control group, n = 24); all individuals under antiretroviral therapy. The genetic diversity, the DN/DS ratio, and the genetic entropy of the first exon of tat were higher in the case group, followed by the positive control group, which was higher than the negative control group. The number of tat codons under positive selection was seven in the case group, six in the positive control group, and one in the negative control group. The prevalence of HIV viral loads below the detection limit was equal in the case and positive control groups, which were lower than in the negative control group. The mean CD4+ T cell counts were higher in the negative control group, followed by the positive control group, and followed by the case group. These results emphasize the negative influence of KSHV in antiretroviral treatment, as well as the HIV‐specific TAT profile among PLHIV who developed KS.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>39092805</pmid><doi>10.1002/jmv.29840</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-9524-0629</orcidid><orcidid>https://orcid.org/0000-0002-8395-7304</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Angiogenesis Anti-Retroviral Agents - therapeutic use Antiretroviral agents Antiretroviral drugs Antiretroviral therapy CD4 antigen CD4 Lymphocyte Count Clonal selection Codons Coinfection - drug therapy Coinfection - virology Endothelial cells Female Genetic diversity Genetic Variation Herpes viruses Herpesvirus 8, Human - genetics HIV HIV Infections - complications HIV Infections - drug therapy HIV Infections - virology HIV-1 - drug effects HIV-1 - genetics HIV‐1 Human immunodeficiency virus Humans Kaposi sarcoma Kaposi Sarcoma‐associated Herpes Virus Kaposi's sarcoma Kaposis sarcoma Lymphocytes Lymphocytes T Male Middle Aged Positive selection Sarcoma Sarcoma, Kaposi - virology tat Tat gene tat Gene Products, Human Immunodeficiency Virus - genetics Tat protein Viral Load |
| title | People living with HIV co‐infected with the Kaposi Sarcoma‐associated Herpes Virus have a distinct HIV Tat profile and higher rates of antiretroviral virologic failure, more evident among those with Kaposi's sarcoma |
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