کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5590722 | 1570157 | 2016 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The well-tempered SIV infection: Pathogenesis of SIV infection in natural hosts in the wild, with emphasis on virus transmission and early events post-infection that may contribute to protection from disease progression
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کلمات کلیدی
CCR5LPSNHPsPTMsTregsRCMGALTSIVRMSTCMTLRs - TLR هاTransmission - انتقالMother-to-infant transmission - انتقال مادر به نوزادMicrobial translocation - انتقال مایکروبیAIDS - ایدزViral loads - بارهای ویروسیAntiretroviral therapy - درمان ضد رتروویروسیrhesus macaques - ریزوس macaquescentral memory T cells - سلول های T حافظه مرکزیRegulatory T cells - سلولهای تی تنظیمکنندهacquired immunodeficiency syndrome - سندرم نقص ایمنی به دست آوردlipopolysaccharide - لیپوپلی ساکاریدNonhuman primates - مقدمه غیر انسانیAfrican green monkeys - میمون های سبز آفریقاییART - هنرhuman immunodeficiency virus - ویروس نقص ایمنی انسانیHIV - ویروس نقص ایمنی انسانی Simian immunodeficiency virus - ویروس کمبود ایمنی سیمانیPathogenesis - پاتونزSMS - پیامکToll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
بوم شناسی، تکامل، رفتار و سامانه شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
African NHPs are infected by over 40 different simian immunodeficiency viruses. These viruses have coevolved with their hosts for long periods of time and, unlike HIV in humans, infection does not generally lead to disease progression. Chronic viral replication is maintained for the natural lifespan of the host, without loss of overall immune function. Lack of disease progression is not correlated with transmission, as SIV infection is highly prevalent in many African NHP species in the wild. The exact mechanisms by which these natural hosts of SIV avoid disease progression are still unclear, but a number of factors might play a role, including: (i) avoidance of microbial translocation from the gut lumen by preventing or repairing damage to the gut epithelium; (ii) control of immune activation and apoptosis following infection; (iii) establishment of an anti-inflammatory response that resolves chronic inflammation; (iv) maintenance of homeostasis of various immune cell populations, including NK cells, monocytes/macrophages, dendritic cells, Tregs, Th17 T-cells, and γδ T-cells; (v) restriction of CCR5 availability at mucosal sites; (vi) preservation of T-cell function associated with down-regulation of CD4 receptor. Some of these mechanisms might also be involved in protection of natural hosts from mother-to-infant SIV transmission during breastfeeding. The difficulty of performing invasive studies in the wild has prohibited investigation of the exact events surrounding transmission in natural hosts. Increased understanding of the mechanisms of SIV transmission in natural hosts, and of the early events post-transmission which may contribute to avoidance of disease progression, along with better comprehension of the factors involved in protection from SIV breastfeeding transmission in the natural hosts, could prove invaluable for the development of new prevention strategies for HIV.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Infection, Genetics and Evolution - Volume 46, December 2016, Pages 308-323
Journal: Infection, Genetics and Evolution - Volume 46, December 2016, Pages 308-323
نویسندگان
Kevin Raehtz, Ivona Pandrea, Cristian Apetrei,