Evolution of genetic diversity and drug resistance mutations in HIV-1 among untreated patients from Mali between 2005 and 2006.
OBJECTIVE
To describe HIV-1 variants circulating in Mali and to estimate the rate of transmission of HIV-1 drug resistance in 2006.


METHODS
Viral reverse transcriptase (RT) and protease (PR) genes from 198 antiretroviral (ARV)-naive patients diagnosed HIV-1 positive in May 2006 in Bamako and Segou were sequenced.


RESULTS
Although CRF02_AG was always the predominant HIV-1 subtype observed (72%), a higher genetic diversity than that in 2005 was observed. The overall prevalence of primary resistance is 11.5% in Mali in 2006, according to the 2007 IAS-USA list of mutations [nucleoside RT inhibitor (NRTI): 1.5%, non-NRTI (NNRTI): 9% and PI: 1%], and 2.5% (NRTI: 1%, NNRTI: 1.5% and PI: 0%), according to the Stanford list of mutations. There was no significant difference between 2005 and 2006 in the overall primary resistance prevalence or in the prevalence of mutations in the different ARV classes. Resistance mutations found in RT and PR genes are in agreement with the highly active antiretroviral therapy regimen available in Mali, except for V90I, V106I and A98G mutations which are associated with etravirine resistance, but polymorphic in non-B subtypes.


CONCLUSIONS
HIV-1 genetic diversity seems increased in Mali, but the overall HIV-1 primary resistance prevalence remains low. This is consistent with the findings from other West African countries where prevalence rates are lower than 5%. However, considering the large scaling up of ARV use in this country, it is necessary to regularly monitor the development of primary resistance in Mali.
UPMC Univ Paris 06, EA2387, 4 Place Jussieu, F-75005 Paris, France.
Anne
A
Derache
Almoustapha-Issiaka
AI
Maiga
Ousmane
O
Traore
Alain
A
Akonde
Mamadou
M
Cisse
Bernard
B
Jarrousse
Victoria
V
Koita
Bah
B
Diarra
Guislaine
G
Carcelain
Francis
F
Barin
Cecilia
C
Pizzocolo
Louis
L
Pizarro
Christine
C
Katlama
Vincent
V
Calvez
Anne-Geneviève
AG
Marcelin
D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy* / Q000635:transmission / Q000821:virology*; D000293:Adolescent; D000328:Adult; D000368:Aged; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002648:Child; D002675:Child, Preschool; D004351:Drug Resistance; D005260:Female; D014644:Genetic Variation; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000145:classification / Q000187:drug effects* / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008302:Mali; D008875:Middle Aged; D008969:Molecular Sequence Data; D020125:Mutation, Missense; D010802:Phylogeny; D012367:RNA, Viral / Q000235:genetics; D017422:Sequence Analysis, DNA
D019380:Anti-HIV Agents; D012367:RNA, Viral; C514824:reverse transcriptase, Human immunodeficiency virus 1; D054303:HIV Reverse Transcriptase; D016333:HIV Protease; C514803:p16 protease, Human immunodeficiency virus 1