The resurgence of SARS in the late December of 2019 due to a novel coronavirus, SARS-CoV-2, has shadowed the world with a pandemic. The physiopathology of this virus is very much in semblance with the previously known SARS-CoV and MERS-CoV. However, the unprecedented transmissibility of SARS-CoV-2 has been puzzling the scientific efforts. Though the virus harbors much of the genetic and architectural features of SARS-CoV, a few differences acquired during its evolutionary selective pressure is helping the SARS-CoV-2 to establish prodigious infection. Making entry into host the cell through already established ACE-2 receptor concerted with the action of TMPRSS2, is considered important for the virus. During the infection cycle of SARS-CoV-2, the innate immunity witnesses maximum dysregulations in its molecular network causing fatalities in aged, comorbid cases. The overt immunopathology manifested due to robust cytokine storm shows ARDS in severe cases of SARS-CoV-2. A delayed IFN activation gives appropriate time to the replicating virus to evade the host antiviral response and cause disruption of the adaptive response as well. We have compiled various aspects of SARS-CoV-2 in relation to its unique structural features and ability to modulate innate as well adaptive response in host, aiming at understanding the dynamism of infection.

2019 年 12 月下旬，新型冠状病毒 SARS-CoV-2 导致 SARS 卷土重来，给世界带来了大流行的阴影。该病毒的病理生理学与之前已知的 SARS-CoV 和 MERS-CoV 非常相似。然而，SARS-CoV-2 前所未有的传播能力一直困扰着科学工作。尽管该病毒具有 SARS-CoV 的大部分遗传和结构特征，但在其进化选择压力过程中获得的一些差异正在帮助 SARS-CoV-2 建立惊人的感染能力。通过已建立的 ACE-2 受体与 TMPRSS2 的作用协同进入宿主细胞，被认为对病毒很重要。在 SARS-CoV-2 的感染周期中，先天免疫的分子网络出现最大程度的失调，导致老年合并症病例死亡。在严重的 SARS-CoV-2 病例中，由于强烈的细胞因子风暴而表现出的明显免疫病理学显示 ARDS。延迟的干扰素激活为复制病毒提供了适当的时间来逃避宿主的抗病毒反应，并导致适应性反应的破坏。我们根据 SARS-CoV-2 独特的结构特征以及调节宿主先天和适应性反应的能力，对 SARS-CoV-2 的各个方面进行了整理，旨在了解感染的动态。