A Review of Strategic Immune Evasion by Influenza Virus and Antiviral Response of Interferon

A. Naveed
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引用次数: 2

Abstract

Influenza virus belongs to the family orthomyxovirida. It is a major pathogen that has wide host range including humans, horses, pigs, mink, marine mammals, felids and a diverse range of domestic birds but shorebirds and wildfowl are considered to be the reservoir host in nature [1]. The influenza virus has an enveloped, segmented genome comprised of eight segments of negative sense-single stranded RNA (-ssRNA). The –ssRNA has coding ability of 11 proteins as Matrix proteins (M1 and M2), Hemagglutinin (HA), Neuraminidase (NA), Nucleocapsid Protein (NP), Polymerase basic protein (PB1, PB2, and PA), PB1-F2 and non-structural proteins (NS1 and NS2) [2]. Based on the surface glycoproteins the Hemagglutinin (HA) and Neuraminidase (NA), influenza viruses are classified into three types A, B and C. Viral entry in the host cell is mediated by receptor binding and membrane fusion activity of HA while NA mediates the release of viral progeny by enzymatic cleavage. The Influenza viruses that represent 16HA and 9NA antigenic subtypes have been identified in poultry and wild birds throughout the world. These antigenic subtypes can be found in different arrangements as H1N1, H16N3 [3]. Hemagglutinins are initially synthesized as a single polypeptide precursor (HA0), later these are cleaved into HA1 and HA2 subunits by proteases. The introduction of influenza virus subtypes H5 and H7 into the poultry is reported to be highly infectious and may cause outbursts of highly pathogenic avian influenza (HPAI, earlier known as B fowl plague) but this is not associated with other HA subtypes [4]. The introduction of basic amino acid residues into the cleavage site of HA0 converts the low pathogenic avian influenza virus to high pathogenic avian influenza virus, this HA0 helps in systemic replication of the virus [5]. The highly pathogenic influenza virus is responsible for the outbursts, as recurrent outbursts were recorded by influenza viruses of subtype H5N1 in Europe, the Middle East, Asia and Africa; H5N2 in Italy, Mexico and Texas; H7N1 in Italy; H7N3 Abstract
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流感病毒战略性免疫逃避及干扰素抗病毒应答研究进展
流感病毒属于正黏液病毒科。它是一种主要的病原体,宿主范围广泛,包括人、马、猪、水貂、海洋哺乳动物、猫科动物和多种家禽,但在自然界中,滨鸟和野禽被认为是水库宿主[1]。流感病毒具有由8段负义单链RNA (-ssRNA)组成的包膜分段基因组。-ssRNA具有编码基质蛋白(M1和M2)、血凝素(HA)、神经氨酸酶(NA)、核衣壳蛋白(NP)、聚合酶碱性蛋白(PB1、PB2和PA)、PB1- f2和非结构蛋白(NS1和NS2)等11种蛋白的能力[2]。根据流感病毒的表面糖蛋白血凝素(HA)和神经氨酸酶(NA),将流感病毒分为A、B和c三种类型。病毒进入宿主细胞是通过HA的受体结合和膜融合活性介导的,而NA通过酶裂解介导病毒子代的释放。代表16HA和9NA抗原亚型的流感病毒已在世界各地的家禽和野生鸟类中被鉴定出来。这些抗原亚型的排列方式不同,如H1N1、H16N3[3]。血凝素最初是作为单个多肽前体(HA0)合成的,随后被蛋白酶裂解为HA1和HA2亚基。据报道,将流感病毒亚型H5和H7引入家禽具有高度传染性,并可能引起高致病性禽流感(HPAI,早期称为B型禽鼠疫)暴发,但这与其他HA亚型无关[4]。将碱性氨基酸残基引入HA0的裂解位点,将低致病性禽流感病毒转化为高致病性禽流感病毒,该HA0有助于病毒的系统复制[5]。高致病性流感病毒是造成疫情的原因,因为在欧洲、中东、亚洲和非洲记录了H5N1亚型流感病毒的反复暴发;意大利、墨西哥和德克萨斯州发现H5N2病毒;意大利发现H7N1病毒;H7N3文摘
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