HIV-1 (人免疫缺陷病毒-1)感染不能將幹擾素導入其所感染的細胞中，但其中所涉及的機制卻沒有被確定。樹突細胞（皮膚、黏膜和淋巴組織中的免疫細胞）調控病原體的先天檢測及在適應性免疫中所涉及的其他免疫細胞的激活，但卻不是為了對付HIV。樹突細胞對HIV感染是有抵抗力的，雖然它們也的確與該病毒結合，並且被認為幫助T-helper細胞的感染。
現在研究表明，當HIV感染的通常阻斷被樹突細胞繞過時（通過暴露於 Vpx accessory 來實現，它是一種來自猴免疫缺陷病毒SIVmac的蛋白），HIV便不會誘導I-型幹擾素響應和T-細胞激發。HIV-1的毒性也許與其能夠通過呆在樹突細胞之外來逃避先天免疫的能力有關，而且這一策略的運用可能有助於疫苗設計。（生物谷Bioon.com）
生物谷推薦英文摘要：
Nature doi:10.1038/nature09337
A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells
Nicolas Manel,Brandon Hogstad,Yaming Wang,David E. Levy,Derya Unutmaz& Dan R. Littmandan.littman
Dendritic cells serve a key function in host defence, linking innate detection of microbes to activation of pathogen-specific adaptive immune responses1, 2. Whether there is cell-intrinsic recognition of human immunodeficiency virus (HIV) by host innate pattern-recognition receptors and subsequent coupling to antiviral T-cell responses is not yet known3. Dendritic cells are largely resistant to infection with HIV-14, but facilitate infection of co-cultured T-helper cells through a process of trans-enhancement5, 6. Here we show that, when dendritic cell resistance to infection is circumvented7, 8, HIV-1 induces dendritic cell maturation, an antiviral type I interferon response and activation of T cells. This innate response is dependent on the interaction of newly synthesized HIV-1 capsid with cellular cyclophilin A (CYPA) and the subsequent activation of the transcription factor IRF3. Because the peptidylprolyl isomerase CYPA also interacts with HIV-1 capsid to promote infectivity, our results indicate that capsid conformation has evolved under opposing selective pressures for infectivity versus furtiveness. Thus, a cell-intrinsic sensor for HIV-1 exists in dendritic cells and mediates an antiviral immune response, but it is not typically engaged owing to the absence of dendritic cell infection. The virulence of HIV-1 may be related to evasion of this response, the manipulation of which may be necessary to generate an effective HIV-1 vaccine.