Murray S M, Picker L J, Axthelm M K, Linial M L
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N., Seattle, WA 98109, USA.
J Virol. 2006 Jan;80(2):663-70. doi: 10.1128/JVI.80.2.663-670.2006.
Foamy viruses (FV) are the oldest known genus of retroviruses and have persisted in nonhuman primates for over 60 million years. FV are efficiently transmitted, leading to a lifelong nonpathogenic infection. Transmission is thought to occur through saliva, but the detailed mechanism is unknown. Interestingly, this persistent infection contrasts with the rapid cytopathicity caused by FV in vitro, suggesting a host defense against FV. To better understand the tissue specificity of FV replication and host immunologic defense against FV cytopathicity, we quantified FV in tissues of healthy rhesus macaques (RM) and those severely immunosuppressed by simian immunodeficiency virus (SIV). Contrary to earlier findings, we find that all immunocompetent animals consistently have high levels of viral RNA in oral tissues but not in other tissues examined, including the small intestine. Strikingly, abundant viral transcripts were detected in the small intestine of all of the SIV-infected RM, which has been shown to be a major site of SIV (and human immunodeficiency virus)-induced CD4+ T-cell depletion. In contrast, there was a trend to lower viral RNA levels in oropharyngeal tissues of SIV-infected animals. The expansion of FV replication to the small intestine but not to other CD4+ T-cell-depleted tissues suggests that factors other than T-cell depletion, such as dysregulation of the jejunal microenvironment after SIV infection, likely account for the expanded tissue tropism of FV replication.
泡沫病毒（FV）是已知最古老的逆转录病毒属，已在非人类灵长类动物中存在超过6000万年。FV能有效传播，导致终身无致病性感染。传播被认为是通过唾液发生的，但具体机制尚不清楚。有趣的是，这种持续性感染与FV在体外引起的快速细胞病变形成对比，提示存在针对FV的宿主防御机制。为了更好地理解FV复制的组织特异性以及宿主针对FV细胞病变的免疫防御，我们对健康恒河猴（RM）以及被猴免疫缺陷病毒（SIV）严重免疫抑制的恒河猴组织中的FV进行了定量分析。与早期研究结果相反，我们发现所有具有免疫活性的动物口腔组织中始终存在高水平的病毒RNA，而在包括小肠在内的其他检测组织中则没有。令人惊讶的是，在所有感染SIV的RM的小肠中都检测到了丰富的病毒转录本，小肠已被证明是SIV（以及人类免疫缺陷病毒）诱导CD4+T细胞耗竭的主要部位。相比之下，感染SIV的动物口咽组织中的病毒RNA水平有降低的趋势。FV复制扩展到小肠但未扩展到其他CD4+T细胞耗竭的组织，这表明除了T细胞耗竭之外的其他因素，如SIV感染后空肠微环境的失调，可能是FV复制组织嗜性扩展的原因。
