Immune escape mutations in HIV-1 controllers in the Brazilian Amazon region

• Autor(a) principal: Gomes, Samara Tatielle Monteiro
• Data de Publicação: 2020
• Outros Autores: Amoras, Ednelza da Silva Graça, Gomes, Érica Ribeiro, Queiroz, Maria Alice Freitas, Sousa Júnior, Edivaldo Costa, Massafra, Janaína Mota de Vasconcelos, Lemos, Poliana da Silva, Vianez Júnior, João Lídio da Silva Gonçalves, Vallinoto, Antonio Carlos Rosário
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Digital do Instituto Evandro Chagas (Patuá)
• Texto Completo: https://patua.iec.gov.br/handle/iec/4142
• topic: HIV-1 / ultraestrutura; Linfócitos T / imunologia; Viremia; Mutação

Background: Human immunodeficiency virus (HIV-1) infection is characterized by high viral replication and a decrease in CD4+ T cells (CD4+TC), resulting in AIDS, which can lead to death. In elite controllers and viremia controllers, viral replication is naturally controlled, with maintenance of CD4+TC levels without the use of antiretroviral therapy (ART). Methods: The aim of the present study was to describe virological and immunological risk factors among HIV-1-infected individuals according to characteristics of progression to AIDS. The sample included 30 treatment-naive patients classified into three groups based on infection duration (> 6 years), CD4+TC count and viral load: (i) 2 elite controllers (ECs), (ii) 7 viremia controllers (VCs) and (iii) 21 nonviremia controllers (NVCs). Nested PCR was employed to amplify the virus genome, which was later sequenced using the Ion PGM platform for subtyping and analysis of immune escape mutations. Results: Viral samples were classified as HIV-1 subtypes B and F. Greater selection pressure on mutations was observed in the group of viremia controllers, with a higher frequency of immunological escape mutations in the genes investigated, including two new mutations in gag. The viral sequences of viremia controllers and nonviremia controllers did not differ significantly regarding the presence of immune escape mutations. Conclusion: The results suggest that progression to AIDS is not dependent on a single variable but rather on a set of characteristics and pressures exerted by virus biology and interactions with immunogenetic host factors.