February 2003
Case Description and Question:
The following case comes from a physician in South Africa:
This HIV-infected boy is nearly six-years-old. He began treatment with d4T/3TC/EFV in July 2001 (CD4 498 (16%) and virus load (VL) 54400 copies/mL). There were major problems with medication adherence. He was next tested in January 2001 (CD4 422 (16%) and VL 19200). After this, we worked closely with the family and resolved the adherence problems. His viral load dropped quite dramatically to 2470 in April 2002, but his CD4 also had decreased to 11% (506). This trend continued and in December 2002 his CD4 had dropped to 9% (446) and his VL was still reasonable at 7920.
HIV genotyping showed the following:
RT mutations: V106M, M184V, M230L
PI mutations: M36I, L63P, I93L
Reported as:
susceptible to ZDV, d4T, all protease inhibitors
low level resistance ddC, ddI, abacavir
high level resistance to 3TC, DLV, EFV, NVP
What treatment regimen would you suggest at this point?
Expert Opinion:
The HIV genotyping results are interesting. The common M184V mutation is present, indicating high-grade resistance to 3TC. Also present is the V106M mutation. This South African boy is very likely to be infected with HIV subtype (clade) C virus. Recently it has been recognized that clade C isolates frequently contain a valine codon 106 polymorphism (GTG) that facilitates a V106M transition after selection with efavirenz (AIDS 17:F1,2003). This V106M mutation confers high-grade class-wide resistance to the nonnucleoside reverse transcriptase inhibitors (including efavirenz and nevirapine). In contrast to the situation with HIV clade C, most clade B isolates contain a different codon 106 polymorphism (GTA) that does not facilitate the V106M transition.
Given the HIV genotyping results, it seems that a change to a protease inhibitor-containing treatment regimen is the best option. I would suggest d4T/ddI plus lopinavir/r (Kaletra).
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