Abstract
HIV related mutations can be associated with decreased susceptibility to antiretrovirals and treatment failures. There is scarce information about HIV mutations in persons failing HIV treatment in North of Brazil. Our aim was to evaluate evolution of HIV subtypes and mutations patterns related to antiretroviral therapy in this region. We investigated HIV resistance profile in adults failing antiretroviral regimen in Northern Brazil from January, 2004, through December, 2013. Genotype data was evaluated through Stanford University algorithm. There were 377 genotypes from different individuals to evaluate. Resistance mutations were similar to worldwide reports and related to antiretroviral exposure. Most prevalent mutations in the reverse transcriptase gene were M184V (80.1%) and K130N (40.6%). Thymidine associated mutations were more frequent in multiexperienced patients. Most common protease mutations were M46I, V82A, I54V, L90M, I84V, M46L, and L76V. Subtype B was the most prevalent (90.7%). There were differences between subtypes B and non-B mutations. We documented for the first time subtypes and patterns of HIV associated mutations in Northern Brazil. A1 subtype was identified for the first time in this area. Depending on drug regimen and how experienced the patient is, an empirical switch of a failing antiretroviral treatment could be a reasonable option.
Highlights
The use of highly active antiretroviral therapy (HAART) has dramatically changed the natural course of HIV infection in little more than 30 years of its existence [1, 2]
The objective of this study was to evaluate the emergence of HIV drug resistance, the possibility of an empirical antiretroviral switch, and patterns associated with circulating subtypes and ARVs utilized in a population in Para, one of the largest states in the North region of Brazil
There were 332 (88.1%), 247 (65.5%), and 164 (43.5%) mutations associated with resistance to nucleoside reverse transcriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors (PIs), respectively
Summary
The use of highly active antiretroviral therapy (HAART) has dramatically changed the natural course of HIV infection in little more than 30 years of its existence [1, 2]. The success of the treatment is closely related to the continuous use of drugs in order to assure persistent plasma viral load (VL) suppression [7, 8]. Treatment success is directly related to adherence to treatment without viral replication in plasma [10]. Incomplete HAART viral suppression (due to adherence problems or low potency of the combined medications) is related to the development of viral failure [11]. The accumulation of mutations further compromises HIV treatment and limits future options if cross-resistance to other ARVs is developed [13, 14]. The persistence or rebound to detectable levels of HIV in plasma could be an early sign of low adherence or the existence of resistance [15]. The longer the patient is exposed to such treatment, the higher will be the chance to accumulate mutations and develop resistance [16]
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