Human Immunodeficiency Virus Type 1 Drug Resistance Mutations in Peripheral Blood Mononuclear Cell Proviral DNA among Antiretroviral Treatment-Naive and Treatment-Experienced Patients from Pune, India

2007 ◽  
Vol 23 (4) ◽  
pp. 489-497 ◽  
Author(s):  
Sourav Sen ◽  
Srikanth P. Tripathy ◽  
Vaishali M. Chimanpure ◽  
Ajit A. Patil ◽  
Rajani D. Bagul ◽  
...  
2004 ◽  
Vol 20 (11) ◽  
pp. 1166-1172 ◽  
Author(s):  
Said H.S. Al Dhahry ◽  
Euan M. Scrimgeour ◽  
Abdul Raouf Al Suwaid ◽  
Mohammed R.M.Y. Al Lawati ◽  
Hussein S. El Khatim ◽  
...  

2003 ◽  
Vol 77 (13) ◽  
pp. 7682-7688 ◽  
Author(s):  
Elizabeth R. Johnston ◽  
Lynn S. Zijenah ◽  
Solomon Mutetwa ◽  
Rami Kantor ◽  
Chonticha Kittinunvorakoon ◽  
...  

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) subtype C viruses have been found to almost exclusively use the chemokine receptor CCR5 as a coreceptor for entry, even in patients with advanced AIDS. We have characterized subtype C virus isolates from 28 patients from Harare, Zimbabwe, 20 of whom were receiving antiretroviral treatment. Virus from 10 of the treated patients induced syncytium formation (SI virus) when cultured with MT2 cells. Only non-syncytium-inducing (NSI) virus was cultured from the peripheral blood mononuclear cells of the eight patients who had not received treatment. The majority of these subtype C SI viruses were capable of using both CCR5 and CXCR4 as coreceptors for viral entry, and the consensus V3 loop sequences from the SI viruses displayed a high net charge compared to those of NSI viruses. While those on treatment had reverse transcriptase (RT) and protease mutations, there was no clear association between RT and protease drug resistance mutations and coreceptor tropism. These results suggest that CXCR4-tropic viruses are present within the quasispecies of patients infected with subtype C virus and that antiretroviral treatment may create an environment for the emergence of CXCR4 tropism.


2021 ◽  
Vol 1 (1) ◽  
pp. 113-123
Author(s):  
Ahmad A. Hachem ◽  
Essa H. Hariri ◽  
Anthony Mansour ◽  
Jacques Mokhbat

Background: Antiretroviral drug resistance remains a significant problem in the clinical management of patients infected with the Human Immunodeficiency Virus type-1. Aim: This study investigates and reports data on the molecular characterization of HIV-1 isolates from patients who are in a state of therapy failure. Methods: This is a retrospective study conducted on 65 patients in therapy failure. Inclusion criteria included patients diagnosed as being in therapy failure between the years 2009 and 2013. We defined ART failure as either a failure to achieve viral suppression or a failure to detect viral loads below 500 copies/mL after virological suppression in at least two plasma samples.  We used the published WHO list for surveillance of transmitted resistance and the Stanford HIV Drug Resistance Database to identify drug resistance mutations. Results: 65% of the participants had at least one drug resistance mutation (DRM). 12% of the population sampled had resistance to only one ART class, 32% presented with resistance to two classes of antiretroviral drugs, and 20% had resistance to all three classes of drugs. The prevalence of nucleoside transcriptase inhibitor (NRTI) mutations was 55%, the most common DRM being M184V. The prevalence of non-nucleoside reverse transcriptase inhibitor (NNRTI) mutations was 58%, with the most common mutation being the K103N mutation. The prevalence of protease inhibitors drug resistance mutations was 23%, with mutations V82A and I47V being present in 10% of the study population. Conclusion: Our study is the first molecular characterization of DRM emergence in HIV-1 strains from patients failing antiretroviral therapy in Lebanon. Continuous monitoring of resistance patterns for HIV in the country is necessary to tackle the emergent drug resistance.


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