A 6-amino acid insertion/deletion polymorphism in the mucin domain of TIM-1 confers protections against HIV-1 infection

2017 ◽  
Vol 19 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Mara Biasin ◽  
Manuela Sironi ◽  
Irma Saulle ◽  
Chiara Pontremoli ◽  
Micaela Garziano ◽  
...  
Author(s):  
João Pereira‐Vaz ◽  
Pedro Crespo ◽  
Luísa Mocho ◽  
Patrícia Martinho ◽  
Teresa Fidalgo ◽  
...  

2002 ◽  
Vol 76 (20) ◽  
pp. 10533-10539 ◽  
Author(s):  
Louis Alexander ◽  
Mary Janette Aquino-DeJesus ◽  
Michael Chan ◽  
Warren A. Andiman

ABSTRACT We studied a 15-year-old girl, patient X, who has maintained consistently low plasma loads of human immunodeficiency virus type 1 (HIV-1) RNA, as well as normal and stable CD4+ T-cell concentrations. She has presented no clinical manifestations of AIDS, despite having only received zidovudine monotherapy for a part of her life. Patient X's HIV-positive mother (patient Y) has also not progressed to AIDS and has never been treated with antiretroviral agents. HIV-1 isolated from patient X replicated poorly in human peripheral blood mononuclear cells (PBMC). In order to map the determinant of the poor growth of patient X's isolate, viral sequences from patient X were determined and examined for insertion or deletion mutations. These sequences contained a two-amino-acid insertion mutation in the Vif gene, which was also observed in uncultured PBMC acquired at different times. Furthermore, Vif sequences harbored by patient Y contained the identical mutation. These observations suggest that polymorphic HIV-1 was transmitted to patient X perinatally 15 years previously and has been maintained since that time. Recombinant HIV-1, engineered with Vif sequences from patient X, replicated in PBMC to levels approximately 20-fold lower than that of wild type. Removal of the insertion mutation from this recombinant restored replication efficiency to wild-type levels, while introduction of the insertion mutation into wild-type Vif sequences resulted in greatly decreased replication. Furthermore, Vif protein from patient X's HIV-1 was aberrantly cleaved, suggesting a mechanism for loss of Vif function. Since HIV-1 containing these sequences replicates poorly, the implication is that the two-amino-acid insertion mutation in Vif contributes significantly to the nonprogressor status of this mother and child. Further studies of these sequences might provide information regarding contributions of Vif structure and/or function to HIV-1 virulence.


Virology ◽  
2007 ◽  
Vol 364 (2) ◽  
pp. 395-406 ◽  
Author(s):  
Marleen C.D.G. Huigen ◽  
Loek de Graaf ◽  
Dirk Eggink ◽  
Rob Schuurman ◽  
Viktor Müller ◽  
...  

2009 ◽  
Vol 46 (2) ◽  
pp. 169-172 ◽  
Author(s):  
João Pereira-Vaz ◽  
Vitor Duque ◽  
Luís Trindade ◽  
José Saraiva-da-Cunha ◽  
António Meliço-Silvestre

2018 ◽  
Author(s):  
João Luís ◽  
Ana Mata ◽  
Nuno Alves ◽  
Carlos Simões ◽  
João Pereira-Vaz ◽  
...  

2011 ◽  
Vol 44 (3) ◽  
pp. 392-394
Author(s):  
Rejane Maria Tommasini Grotto ◽  
Sílvia Maria Corvino ◽  
Lilian da Silva Reis Munhoz ◽  
Cibele Gomes Ghedini ◽  
Maria Inês de Moura Campos Pardini

Amino acid insertions in the protease have rarely been described in HIVinfected patients. One of these insertions has recently been described in codon 35, although its impact on resistance remains unknown. This study presents a case of an HIV variant with an insertion in codon 35 of the protease, described for the first time in Bauru, State of Sao Paulo, Brazil, circulating in a 38-year-old caucasian male with asymptomatic HIV infection since 1997. The variant isolated showed a codon 35 insertion of two amino acids in the protease: a threonine and an aspartic acid, resulting in the amino acid sequence E35E_TD.


Virology ◽  
2016 ◽  
Vol 498 ◽  
pp. 149-163 ◽  
Author(s):  
Yaqiong Wang ◽  
Zekun Wang ◽  
Ankita Pramanik ◽  
Mario L. Santiago ◽  
Jianming Qiu ◽  
...  

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