2012年8月20日 訊 /生物谷BIOON/ --巨細(xì)胞病毒（CMV）是皰疹病毒的一種，盡管很多人會(huì)攜帶該病毒長(zhǎng)達(dá)一生時(shí)間,，但是該病毒幾乎不會(huì)使攜帶者致病,。近日，來自德國(guó)亥姆霍茲傳染病研究中心和美國(guó)的研究人員揭示了攜帶CMV長(zhǎng)時(shí)間后所引發(fā)的長(zhǎng)期效應(yīng),，研究者表示,，病毒攜帶者在晚年的時(shí)候，其機(jī)體的免疫系統(tǒng)的大量免疫細(xì)胞就會(huì)集中“監(jiān)視”CMV病毒,，因此對(duì)于其它病毒的監(jiān)視抵御能力就會(huì)降低,。這項(xiàng)研究解釋了為什么老年人相比年輕人更易于患感染性疾病。
病毒學(xué)家Luka Cicin-Sain教授是這項(xiàng)研究的主要領(lǐng)導(dǎo)者,，其將這項(xiàng)最近研究成果刊登在了國(guó)際著名雜志PLoS Pathogens上,。文章中，研究者揭示了感染CMV數(shù)月之后,，小鼠和人類一樣,，也表現(xiàn)出了對(duì)其它病毒如流感病毒低的免疫監(jiān)視和抵御能力。
許多成年個(gè)體感染了CMV之后并不會(huì)被發(fā)現(xiàn),，通常也不會(huì)有什么影響,，因?yàn)樵诖蠖鄶?shù)感染病例中，巨細(xì)胞病毒并不會(huì)引發(fā)感染者患病,。僅僅像免疫系統(tǒng)低下的人群,，比如器官接收者、HIV感染者或者剛出生的嬰兒,，這種CMV的感染才是比較危險(xiǎn)的,。另外在每一個(gè)人機(jī)體中，病毒會(huì)變得有潛伏性和持續(xù)性,，但是其始終被控制在一定的水平之內(nèi),。
在年輕人機(jī)體中免疫系統(tǒng)的持續(xù)激活是非常有益的，因?yàn)榧せ畹拿庖呦到y(tǒng)可以抵御入侵機(jī)體的任何感染,。但是再長(zhǎng)的蠟燭也有熄滅的一天,，人類的免疫系統(tǒng)也不例外，隨著年齡增長(zhǎng),，機(jī)體的免疫系統(tǒng)功能會(huì)慢慢下降,。在老年人體內(nèi)，免疫系統(tǒng)會(huì)失去功能,，因此保護(hù)機(jī)體的能力也會(huì)慢慢喪失,，免疫保護(hù)可以用免疫風(fēng)險(xiǎn)預(yù)測(cè)（Immune risk profile,，IRP）來表示，在很多研究中,，研究者研究者研究者IRP和CMV存在之間的關(guān)系,，然而到現(xiàn)在為止，研究者并不清楚IRP是否是CMV感染的結(jié)果抑或者是IRP導(dǎo)致了機(jī)體對(duì)CMV感染敏感性的增加,。
研究者的研究揭示了持續(xù)的CMV的存在可以促使免疫系統(tǒng)“老齡化”,，當(dāng)然除了CMV的感染，機(jī)體的免疫系統(tǒng)也會(huì)慢慢“老齡化”,。從另一方便說,，CMV是機(jī)體中外來的“客人”，人類機(jī)體免疫系統(tǒng)的T細(xì)胞必須時(shí)刻“盯緊”CMV的一舉一動(dòng),。通過在小鼠中進(jìn)行研究表明,，小鼠感染CMV時(shí)間越長(zhǎng)，機(jī)體免疫系統(tǒng)參與監(jiān)視該病毒的時(shí)間越長(zhǎng),，相比抵御其它病原菌的能力和時(shí)間就相應(yīng)縮短了,。而且感染CMV的小鼠不會(huì)對(duì)其它的感染（如流感等）做出任何反應(yīng)。
研究者表示,，我們認(rèn)為淋巴結(jié)中存在的大量的針對(duì)CMV特異性的T細(xì)胞很有可能損傷了免疫系統(tǒng)其余細(xì)胞的激活,。我們的研究揭示了開發(fā)出針對(duì)巨細(xì)胞病毒的疫苗的重要性，盡管其對(duì)我們的健康并無任何直接影響,。（生物谷Bioon.com）
編譯自：Virus Throws a Wrench in the Immune System
doi:10.1371/journal.ppat.1002849
PMC:
PMID:
Cytomegalovirus Infection Impairs Immune Responses and Accentuates T-cell Pool Changes Observed in Mice with Aging
Luka Cicin-Sain1,2*, James D. Brien2,3, Jennifer L. Uhrlaub2,4, Anja Drabig1, Thomas F. Marandu1, Janko Nikolich-Zugich2,4*
Prominent immune alterations associated with aging include the loss of naïve T-cell numbers, diversity and function. While genetic contributors and mechanistic details in the aging process have been addressed in multiple studies, the role of environmental agents in immune aging remains incompletely understood. From the standpoint of environmental infectious agents, latent cytomegalovirus (CMV) infection has been associated with an immune risk profile in the elderly humans, yet the cause-effect relationship of this association remains unclear. Here we present direct experimental evidence that mouse CMV (MCMV) infection results in select T-cell subset changes associated with immune aging, namely the increase of relative and absolute counts of CD8 T-cells in the blood, with a decreased representation of the naïve and the increased representation of the effector memory blood CD8 T-cells. Moreover, MCMV infection resulted in significantly weaker CD8 responses to superinfection with Influenza, Human Herpes Virus I or West-Nile-Virus, even 16 months following MCMV infection. These irreversible losses in T-cell function could not be observed in uninfected or in vaccinia virus-infected controls and were not due to the immune-evasive action of MCMV genes. Rather, the CD8 activation in draining lymph nodes upon viral challenge was decreased in MCMV infected mice and the immune response correlated directly to the frequency of the naïve and inversely to that of the effector cells in the blood CD8 pool. Therefore, latent MCMV infection resulted in pronounced changes of the T-cell compartment consistent with impaired naïve T-cell function.
