Chenine Agnès-Laurence, Buckley Kathleen A, Li Pei-Lin, Rasmussen Robert A, Ong Helena, Jiang Shisong, Wang Tao, Augostini Peter, Secor W Evan, Ruprecht Ruth M
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, Massachusetts 02115-6084, USA.
AIDS. 2005 Nov 4;19(16):1793-7. doi: 10.1097/01.aids.0000189857.51935.0b.
To evaluate the hypothesis that parasitic infections that induce T-helper type 2 (Th2) immune responses, such as schistosomiasis, upregulate HIV-1 replication.
The effect of concomitant Schistosoma mansoni infection was tested in a primate model of acute and chronic simian-human immunodeficiency virus (SHIV) infection in rhesus macaques using a novel SHIV strain encoding the R5 env gene of a primary HIV clade C isolate from sub-Saharan Africa.
S. mansoni-infected rhesus macaques and controls were exposed to SHIV to assess the effects of schistosomiasis on acute viral infection. Effects on chronic viral infection were evaluated by exposing virus-infected animals to parasites. S. mansoni infection was confirmed by the presence of parasite eggs in stool and eosinophilia. Viral RNA loads, cytokine and chemokine mRNA expression were measured by real time reverse transcription-PCR.
S. mansoni coinfection increased the expression of Th2-associated cytokine responses and SHIV replication during both acute and chronic phases of SHIV infection.
These results support the hypothesis that concomitant schistosomiasis upregulates replication of immunodeficiency viruses in coinfected hosts, raising the possibility that parasite-infected individuals may also be more susceptible to acquisition of HIV-1 infection.
评估如下假说,即诱导2型辅助性T细胞(Th2)免疫反应的寄生虫感染,如血吸虫病,会上调HIV-1复制。
使用一种编码来自撒哈拉以南非洲的原发性HIV C亚型分离株R5 env基因的新型猿猴-人类免疫缺陷病毒(SHIV)毒株,在恒河猴急性和慢性猿猴-人类免疫缺陷病毒(SHIV)感染的灵长类动物模型中,测试曼氏血吸虫合并感染的影响。
将感染曼氏血吸虫的恒河猴和对照组暴露于SHIV,以评估血吸虫病对急性病毒感染的影响。通过将病毒感染的动物暴露于寄生虫来评估对慢性病毒感染的影响。通过粪便中存在寄生虫卵和嗜酸性粒细胞增多来确认曼氏血吸虫感染。通过实时逆转录PCR测量病毒RNA载量、细胞因子和趋化因子mRNA表达。
在SHIV感染的急性和慢性阶段,曼氏血吸虫合并感染均增加了Th2相关细胞因子反应的表达和SHIV复制。
这些结果支持如下假说,即合并血吸虫病会上调合并感染宿主中免疫缺陷病毒的复制,增加了寄生虫感染个体可能也更容易感染HIV-1的可能性。