Immune responses and pathogenesis of SARS-CoV-2 during an outbreak in Iran: Comparison with SARS and MERS

Abstract

The beginning of 2020 has seen the emergence of COVID-19, an outbreak caused by a novel coronavirus, SARS-CoV-2, an important pathogen for humans. There is an urgent need to better understand this new virus and to develop ways to control its spread. In Iran, the first case of the COVID-19 was reported after spread from China and other countries. Fever, cough, and fatigue were the most common symptoms of this virus. In worldwide, the incubation period of COVID-19 was 3 to 7 days and approximately 80% of infections are mild or asymptomatic, 15% are severe, requiring oxygen, and 5% are critical infections, requiring ventilation. To mount an antiviral response, the innate immune system recognizes molecular structures that are produced by the invasion of the virus. COVID-19 infection induces IgG antibodies against N protein that can be detected by serum as early as day 4 after the onset of disease and with most patients seroconverting by day 14. Laboratory evidence of clinical patients showed that a specific T-cell response against SARS-CoV-2 is important for the recognition and killing of infected cells, particularly in the lungs of infected individuals. At present, there is no specific antiviral therapy for COVID-19 and the main treatments are supportive. In this review, we investigated the innate and acquired immune responses in patients who recovered from COVID-19, which could inform the design of prophylactic vaccines and immunotherapy for the future.

Keywords: 2019-nCoV disease; B cell; COVID-19; SARS-CoV-2; T cell; coronavirus; immunity.

FIGURE 1

Comparative data of A, confirmed cases, deaths, recovery in Iran until 2020/19/03, and B, mortality rate of COVID‐19 infection in Iran and other countries (Numbers on Venn diagram represent death/confirmed cases.)

FIGURE 2

The genomic structure and phylogenetic tree of coronavirus SARS‐CoV‐2. A, The genome structure of the new coronavirus. B, The phylogenetic tree of representatives from different countries

FIGURE 3

Host immune responses during SARS‐CoV‐2 infection. Airborne SARS‐CoV‐2 leads to infection of ACE2 expressing target cells such as alveolar type 2 cells or other unknown target cells. Cells infected by the virus may escape IFN I resulting in uncontrolled viral replication. The recruitment of neutrophils and monocytes/macrophages is by chemotaxis of pro‐inflammatory cytokines. The “CRS” production‐specific Th1/Th17 may cause immunopathologic injury in the lung that leads to pneumonia. B cells or plasma cells produce SARS‐CoV‐2 specific antibodies that may help neutralize viruses. ²⁵ Lymphopenia caused by viral infections such as SARS‐CoV‐2 can occur with three mechanisms: The first mechanism is the reduction of lymphocyte production or impaired lymphopoiesis. The second mechanism is apoptosis and destruction of lymphocytes. The third mechanism that reduces lymphopenia without decreasing production or increasing degradation is lymphocyte redistribution, such as lymphocyte attachment to the vascular endothelium (a phenomenon similar to neutrophil marginalization) that can lead to decrease in circulating lymphocytes