Do Blood Phenotypes of Feline AB Blood Group System Affect the SARS-CoV-2 Antibody Serostatus in Cats?

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Abstract

Cats are susceptible to coronavirus infections, including infection by human severe acute respiratory syndrome coronavirus (SARS-CoV). In human ABO system blood groups, alloantibodies can play a direct role in resistance to infectious diseases. Individuals with the AB blood type were over-represented in the SARS-CoV-2 infection group. Blood type AB individuals lack both anti-A and anti-B antibodies, and therefore lack the protective effect against SARS-CoV-2 infection given by these antibodies. Starting from this knowledge, this pilot preliminary study evaluated a possible association between feline blood phenotypes A, B, and AB and serostatus for SARS-CoV-2 antibodies in cats. We also investigated selected risk or protective factors associated with seropositivity for this coronavirus. A feline population of 215 cats was analysed for AB group system blood phenotypes and antibodies against the nucleocapsid (N-protein) SARS-CoV-2 antigen using a double antigen ELISA. SARS-CoV-2 seropositive samples were confirmed using a surrogate virus neutralization test (sVNT). Origin (stray colony/shelter/owned cat), breed (DSH/non DSH), gender (male/female), reproductive status (neutered/intact), age class (kitten/young adult/mature adult/senior), retroviruses status (seropositive/seronegative), and blood phenotype (A, B, and AB) were evaluated as protective or risk factors for SARS-CoV-2 seropositivity. Seropositivity for antibodies against the SARS-CoV-2 N-protein was recorded in eight cats, but only four of these tested positive with sVNT. Of these four SARS-CoV-2 seropositive cats, three were blood phenotype A and one was phenotype AB. Young adult age (1–6 years), FeLV seropositivity and blood type AB were significantly associated with SARS-CoV-2 seropositivity according to a univariate analysis, but only blood type AB (p = 0.0344, OR = 15.4, 95%CI: 1.22–194.39) and FeLV seropositivity (p = 0.0444, OR = 13.2, 95%CI: 1.06–163.63) were significant associated risk factors according to a logistic regression. Blood phenotype AB might be associated with seropositivity for SARS-CoV-2 antibodies. This could be due, as in people, to the protective effect of naturally occurring alloantibodies to blood type antigens which are lacking in type AB cats. The results of this pilot study should be considered very preliminary, and we suggest the need for further research to assess this potential relationship.

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A pneumonia outbreak associated with a new coronavirus of probable bat origin

Peng Zhou, Xing-Lou Yang, Xian-Guang Wang … (2020)

Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.

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Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses

Michael Letko, Andrea Marzi, Vincent Munster (2020)

Over the past 20 years, several coronaviruses have crossed the species barrier into humans, causing outbreaks of severe, and often fatal, respiratory illness. Since SARS-CoV was first identified in animal markets, global viromics projects have discovered thousands of coronavirus sequences in diverse animals and geographic regions. Unfortunately, there are few tools available to functionally test these viruses for their ability to infect humans, which has severely hampered efforts to predict the next zoonotic viral outbreak. Here, we developed an approach to rapidly screen lineage B betacoronaviruses, such as SARS-CoV and the recent SARS-CoV-2, for receptor usage and their ability to infect cell types from different species. We show that host protease processing during viral entry is a significant barrier for several lineage B viruses and that bypassing this barrier allows several lineage B viruses to enter human cells through an unknown receptor. We also demonstrate how different lineage B viruses can recombine to gain entry into human cells, and confirm that human ACE2 is the receptor for the recently emerging SARS-CoV-2.

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Genomewide Association Study of Severe Covid-19 with Respiratory Failure

David Ellinghaus, Frauke Degenhardt, Luis Bujanda … (2020)

Abstract Background There is considerable variation in disease behavior among patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (Covid-19). Genomewide association analysis may allow for the identification of potential genetic factors involved in the development of Covid-19. Methods We conducted a genomewide association study involving 1980 patients with Covid-19 and severe disease (defined as respiratory failure) at seven hospitals in the Italian and Spanish epicenters of the SARS-CoV-2 pandemic in Europe. After quality control and the exclusion of population outliers, 835 patients and 1255 control participants from Italy and 775 patients and 950 control participants from Spain were included in the final analysis. In total, we analyzed 8,582,968 single-nucleotide polymorphisms and conducted a meta-analysis of the two case–control panels. Results We detected cross-replicating associations with rs11385942 at locus 3p21.31 and with rs657152 at locus 9q34.2, which were significant at the genomewide level (P<5×10−8) in the meta-analysis of the two case–control panels (odds ratio, 1.77; 95% confidence interval [CI], 1.48 to 2.11; P=1.15×10−10; and odds ratio, 1.32; 95% CI, 1.20 to 1.47; P=4.95×10−8, respectively). At locus 3p21.31, the association signal spanned the genes SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6 and XCR1. The association signal at locus 9q34.2 coincided with the ABO blood group locus; in this cohort, a blood-group–specific analysis showed a higher risk in blood group A than in other blood groups (odds ratio, 1.45; 95% CI, 1.20 to 1.75; P=1.48×10−4) and a protective effect in blood group O as compared with other blood groups (odds ratio, 0.65; 95% CI, 0.53 to 0.79; P=1.06×10−5). Conclusions We identified a 3p21.31 gene cluster as a genetic susceptibility locus in patients with Covid-19 with respiratory failure and confirmed a potential involvement of the ABO blood-group system. (Funded by Stein Erik Hagen and others.)