HIV-1 (人免疫缺陷病毒-1)感染不能將干擾素導(dǎo)入其所感染的細(xì)胞中,，但其中所涉及的機(jī)制卻沒(méi)有被確定,。樹(shù)突細(xì)胞（皮膚,、粘膜和淋巴組織中的免疫細(xì)胞）調(diào)控病原體的先天檢測(cè)及在適應(yīng)性免疫中所涉及的其他免疫細(xì)胞的激活,，但卻不是為了對(duì)付HIV,。樹(shù)突細(xì)胞對(duì)HIV感染是有抵抗力的,，雖然它們也的確與該病毒結(jié)合,，并且被認(rèn)為幫助T-helper細(xì)胞的感染。
現(xiàn)在研究表明,，當(dāng)HIV感染的通常阻斷被樹(shù)突細(xì)胞繞過(guò)時(shí)（通過(guò)暴露于 Vpx accessory 來(lái)實(shí)現(xiàn),，它是一種來(lái)自猴免疫缺陷病毒SIVmac的蛋白），HIV便不會(huì)誘導(dǎo)I-型干擾素響應(yīng)和T-細(xì)胞激發(fā),。HIV-1的毒性也許與其能夠通過(guò)呆在樹(shù)突細(xì)胞之外來(lái)逃避先天免疫的能力有關(guān),，而且這一策略的運(yùn)用可能有助于疫苗設(shè)計(jì)。（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.
