Prolonged tenofovir treatment of macaques infected with K65R reverse transcriptase mutants of SIV results in the development of antiviral immune responses that control virus replication after drug withdrawal

Table 1 Summary of history of tenofovir-treated SIV-infected macaques

Animal number	Virus inoculum^a	Age of virus infection	Start of tenofovir^{b, c}	CD8+ cell depletion^d	Temporary tenofovir interruption	Permanent tenofovir withdrawal	Time of euthanasia
29276	SIVmac-K65R	3 days	3 wks	316 wks	None	None	736 wks
30577	RT-SHIV	19 months	20 wks	263 wks	289 to 298 wks	552 wks	595 wks
32186	SIVmac251	17 months	2 wks	39 wks	64 to 71 wks	457 wks	498 wks
33088	SIVmac251	12 months	2 wks	2 wks	32 to 39 wks	425 wks	468 wks
33091	SIVmac251	12 months	2 wks	2 wks	32 to 39 wks	425 wks	466 wks

^a Animals were inoculated orally or intravenously with wild-type SIVmac251 or RT-SHIV, with the exception of animal 29276, which was inoculated with a K65R SIV isolate (SIVmac385) derived from tenofovir-treated SIVmac251-infected animals, as described previously [10, 11, 13]. All animals had reached undetectable viremia (with sometimes transient blips). With exception of animal 33091, which eventually had a gradual increase in viremia, all other animals maintained undetectable or low viremia even after tenofovir withdrawal.
^b Tenofovir was initially given to all these animals at a once-daily regimen of 30 mg/kg body weight, administered subcutaneously, with subsequent dosage reductions to stable maintenance regimens, as described earlier [10, 13, 15].
^c Times are expressed as weeks after SIV inoculation.
^d Transient CD8+ cell depletion was performed by administration of the monoclonal antibody cM-T807 as described earlier [11].

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