key: cord-354101-8a7tohcx authors: Silva de Oliveira, Daniela; Medeiros, Nayara I.; Gomes, Juliana A.S. title: Immune response in COVID-19: What do we currently know? date: 2020-09-09 journal: Microb Pathog DOI: 10.1016/j.micpath.2020.104484 sha: doc_id: 354101 cord_uid: 8a7tohcx In 2002/2003 there was a pandemic denominate SARS (severe acute respiratory syndrome), caused by the SARS-CoV virus that belongs to the genera Betacoranavirus and the family Coronaviridae, generally responsible for influenza infections. In mid of 2019, a new disease by the coronavirus named by COVID-19 (SARS-CoV-2) emerged, both infections have flu symptoms, however they are infections that variable intensity, being medium to severe. In medium infections individuals have the virus and exhibit symptoms, however hospitalization is not necessary, in severe infections, individuals are hospitalized, have high pathology and in some cases progress to death. The virus is formed by simple positive RNA, enveloped, non-segmented, and presenting the largest genome of viruses constituting 32 Kb, consisting of envelope proteins, membrane, nucleocapsid and spike protein, which is essential in the interaction with the host cells. As for the origin of this virus, research has been intensified to determine this paradox and although the similarity with SARS-CoV, this virus did not has necessarily the same place of origin. As for the immune system, it is currently unknown how this new virus interacts. In this brief review, we demonstrate important considerations about the responses to this infection. The acute respiratory syndrome is a disease caused by the SARS-CoV-2 virus (COVID-37 19), where symptoms include difficulty breathing, high fever, and cough (WHO, 2020). Integrated analyses of single-cell atlases reveal age, gender, and 668 smoking status associations with cell type-specific expression of mediators of SARS-669 CoV-2 viral entry and highlights inflammatory programs in putative target 670 cells Clinicopathologic, immunohistochemical, and ultrastructural findings of 673 a fatal case of Middle East respiratory syndrome coronavirus infection in the United 674 Arab Emirates Lung pathology of fatal severe acute respiratory syndrome Remembrance of things past: long-term B cell memory 683 after infection and vaccination Pathogenic human coronavirus infections: causes and consequences of 689 cytokine storm and immunopathology Severe acute respiratory syndrome T cell responses: naive to memory and everything in between Immune responses in COVID-19 700 and potential vaccines: Lessons learned from SARS and MERS epidemic Middle East respiratory syndrome coronavirus A review. Germs, v. 9 Immune responses and pathogenesis of 707 SARS-CoV-2 during an outbreak in Iran: Comparison with SARS and 708 MERS Immunity and immunopathology to viruses: what 711 decides the outcome? 15 drugs being tested to treat COVID-19 and how they would 717 work. Nature medicine WHO-World Health Organization. Coronavirus disease. Coronavírus disease (COVID-762 19) outbreak situation Middle East respiratory syndrome coronavirus 766 (MERS-CoV) sheets/detail/middle-east-respiratory-syndrome-coronavirus-(mers-cov)> Access WHO-World Health Organization. Mers situation update Q&A on coronaviruses (COVID-19). Available in: 775 < WHO-World Health Organization. DRAFT landscape of COVID-19 candidate 779 vaccines-2 detail/draft-landscape-of-covid-19-candidate-vaccines> Neutralizing antibody responses to SARS-CoV-2 in a COVID-19 783 recovered patient cohort and their implications Pathological findings of COVID-19 associated with acute respiratory 786 distress syndrome. The Lancet respiratory medicine The anticoagulant nafamostat potently inhibits SARS-CoV-2 789 infection in vitro: an existing drug with multiple possible therapeutic 790 effects. bioRxiv