Expression data from SIVagm-infected African green monkeys (Chlorocebus sabaeus). Chlorocebus sabaeus

In contrast to SIVagm, which does not cause disease in its natural simian host, HIV-1 expresses the accessory protein Vpu and encodes a Nef protein that fails to suppress T cell activation via down-modulation of CD3. Although both, Vpu and Nef have been implicated as pathogenicity determinants, their relevance for viral replication and disease progression in vivo has remained unclear. Here, we analyzed gene expression in African green monkeys infected with SIVagm chimeras differing in their expression of nef and/or vpu. We used microarrays to analyze global gene expression of African green monkeys in response to infection with SIVagm and found that the viral accessory nef and vpu genes co-determine the induction of distinct gene sets. Overall design: Twelve juvenile female AGMs (Chlorocebus sabaeus) were randomly distributed to four groups with three monkeys each. The monkeys were infected with wild type SIVagm (WT; monkeys #14623, 14625, 14629), a chimera expressing SIVgsn Vpu (GU; #14624, 14627, 14632); a chimera expressing HIV-1 Nef (1N; #14626, 14630, 14631); or a double chimera expressing both SIVgsn Vpu and HIV-1 Nef (GU1N; #14628, 14633, 14634). RNA was isolated from whole blood 170 weeks post infection and whole genome microarray analysis was performed.

与在其自然猴类宿主中不引发疾病的猿猴免疫缺陷病毒非洲绿猴株（SIVagm）不同，人类免疫缺陷病毒1型（HIV-1）表达辅助蛋白病毒蛋白U（Vpu），且编码无法通过下调分化簇3（CD3）抑制T细胞活化的负调控因子（Nef）。尽管Vpu与Nef均被认定为致病性决定因子，但二者在体内对病毒复制及疾病进展的相关性仍未明确。
本研究针对感染了nef和/或vpu基因表达存在差异的SIVagm嵌合体的非洲绿猴（AGMs）的基因表达情况展开分析。通过微阵列技术分析非洲绿猴感染SIVagm后的全基因组基因表达谱，本研究发现病毒辅助基因nef与vpu共同调控不同基因集的诱导表达。
实验设计：将12只幼年雌性萨巴埃绿猴（Chlorocebus sabaeus）随机分为4组，每组3只。实验猴分别感染野生型SIVagm（WT；猴编号#14623、14625、14629）、表达SIVgsn Vpu的嵌合病毒（GU；#14624、14627、14632）、表达HIV-1 Nef的嵌合病毒（1N；#14626、14630、14631），以及同时表达SIVgsn Vpu与HIV-1 Nef的双嵌合病毒（GU1N；#14628、14633、14634）。于感染后170周采集全血样本分离RNA，并开展全基因组微阵列分析。