Medical Microbiology and Immunology最新文献

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The quantity and quality of anti-SARS-CoV-2 antibodies show contrariwise association with COVID-19 severity: lessons learned from IgG avidity. 抗sars - cov -2抗体的数量和质量与COVID-19严重程度呈相反相关:从IgG贪婪中吸取的教训
IF 5.4 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-06-01 DOI: 10.1007/s00430-023-00763-y
Mehrdad Hajilooi, Fariba Keramat, Akram Moazenian, Mohsen Rastegari-Pouyani, Ghasem Solgi
{"title":"The quantity and quality of anti-SARS-CoV-2 antibodies show contrariwise association with COVID-19 severity: lessons learned from IgG avidity.","authors":"Mehrdad Hajilooi,&nbsp;Fariba Keramat,&nbsp;Akram Moazenian,&nbsp;Mohsen Rastegari-Pouyani,&nbsp;Ghasem Solgi","doi":"10.1007/s00430-023-00763-y","DOIUrl":"https://doi.org/10.1007/s00430-023-00763-y","url":null,"abstract":"<p><p>Gaining more appreciation on the protective/damaging aspects of anti-SARS-CoV-2 immunity associated with disease severity is of great importance. This study aimed to evaluate the avidity of serum IgG antibodies against SARS-CoV-2 spike (S) and nucleocapsid (N) in hospitalized symptomatic COVID-19 patients and asymptomatic RT-PCR-confirmed SARS-CoV-2 carriers as well as to compare antibody avidities with respect to vaccination status, vaccination dose and reinfection status. Serum levels of anti-S and anti-N IgG were determined using specific ELISA kits. Antibody avidity was determined by urea dissociation assay and expressed as avidity index (AI) value. Despite higher IgG levels in the symptomatic group, AI values of both anti-S and anti-N IgG were significantly lower in this group compared to asymptomatic individuals. In both groups, anti-S AI values were elevated in one-dose and two-dose vaccinees versus unvaccinated subjects, although significant differences were only detected in the symptomatic group. However, anti-N avidity showed no significant difference between the vaccinated and unvaccinated subgroups. Almost all vaccinated patients of different subgroups (based on vaccine type) had higher anti-S IgG avidity, while the statistical significance was detected only between those receiving Sinopharm compared to the unvaccinated subgroup. Also, statistically significant differences in antibody AIs were only found between primarily infected individuals of the two groups. Our findings indicate a key role for anti-SARS-CoV-2 IgG avidity in protection from symptomatic COVID-19 and calls for the incorporation of antibody avidity measurement into the current diagnostic tests to predict effective immunity toward SARS-CoV-2 infection or even for prognostic purposes.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 3","pages":"203-220"},"PeriodicalIF":5.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10133916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Association of IFIH1 and DDX58 genes polymorphism with susceptibility to COVID-19. IFIH1和DDX58基因多态性与COVID-19易感性的关系
IF 5.4 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-06-01 Epub Date: 2023-06-13 DOI: 10.1007/s00430-023-00764-x
Parisa Feizollahi, Mohammad Hossein Zamanian, Sara Falahi, Farhad Salari, Zahra Mahmoudi, Elham Faryadi, Ali Gorgin Karaji, Alireza Rezaiemanesh
{"title":"Association of IFIH1 and DDX58 genes polymorphism with susceptibility to COVID-19.","authors":"Parisa Feizollahi, Mohammad Hossein Zamanian, Sara Falahi, Farhad Salari, Zahra Mahmoudi, Elham Faryadi, Ali Gorgin Karaji, Alireza Rezaiemanesh","doi":"10.1007/s00430-023-00764-x","DOIUrl":"10.1007/s00430-023-00764-x","url":null,"abstract":"<p><p>Pattern recognition receptors of the innate immune system, such as RIG-I and MDA5, are responsible for recognizing viruses and inducing interferon production. Genetic polymorphisms in the coding regions of RLR may be associated with the severity of COVID-19. Considering the contribution of the RLR signaling in immune-mediated reactions, this study investigated the association between three SNP in the coding region of IFIH1 and DDX58 genes with the susceptibility to COVID-19 in the Kermanshah population, Iran. 177 patients with severe and 182 with mild COVID-19 were admitted for this study. Genomic DNA was extracted from peripheral blood leukocytes of patients to determine the genotypes of two SNPs, rs1990760(C>T) and rs3747517(T>C) IFIH1 gene and rs10813831(G>A) DDX58 gene using PCR-RFLP method. Our results showed that the frequency of the AA genotype of rs10813831(G>A) was associated with susceptibility to COVID-19 compared to the GG genotype (p = 0.017, OR = 2.593, 95% CI 1.173-5.736). We also observed a statistically significant difference in the recessive model for SNPs rs10813831 variant (AA versus GG + GA, p = 0.003, OR = 2.901, 95% CI 1.405-6.103). Furthermore, No significant association was found between rs1990760 (C>T) and rs3747517(T>C) of IFIH1 gene polymorphisms with COVID-19. Our findings suggest that DDX58 rs10813831(A>G) polymorphism may be associated with COVID-19 severity in the Kermanshah population, Iran.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 3","pages":"221-229"},"PeriodicalIF":5.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Phenotypic and genotypic identification of carbapenem resistance in Bacteroides fragilis clinical strains. 脆弱拟杆菌临床菌株碳青霉烯类耐药表型及基因型鉴定。
IF 5.4 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-06-01 DOI: 10.1007/s00430-023-00765-w
Marta Kierzkowska, Anna Majewska, Konrad Karłowicz, Hanna Pituch
{"title":"Phenotypic and genotypic identification of carbapenem resistance in Bacteroides fragilis clinical strains.","authors":"Marta Kierzkowska,&nbsp;Anna Majewska,&nbsp;Konrad Karłowicz,&nbsp;Hanna Pituch","doi":"10.1007/s00430-023-00765-w","DOIUrl":"https://doi.org/10.1007/s00430-023-00765-w","url":null,"abstract":"<p><p>Bacteroides fragilis is an important etiological agent of serious infections in humans. Rapid methods, readily adaptable to use in medical laboratories, are needed to detect antibiotic resistance and decrease the likelihood of therapy failure. The aim of this study was to determine the prevalence of B. fragilis cfiA-positive isolates. The second purpose was to investigate the carbapenemase activity in B. fragilis strains by Carba NP test. In the study, 5.2% of B. fragilis isolates are phenotypically resistant to meropenem. The cfiA gene was identified in 6.1% of B. fragilis isolates. The MICs of meropenem were significantly higher in cfiA-positive strains. The presence of the cfiA gene along with the IS1186 was detected in one B. fragilis strain which was resistant to meropenem (MIC 1.5 mg/L). The Carba NP test results were positive for all the cfiA-positive strains, including those susceptible to carbapenems based on their MIC values. A review of the literature revealed that the rate of B. fragilis with the cfiA gene varies from 7.6 to 38.9% worldwide. Presented results are in line with the other European studies. Phenotypic testing with the Carba NP test, it seems to be a viable alternative for the cfiA gene detection in B. fragilis isolates. The positive result obtained is of greater clinical importance than the detection of the gene cfiA.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 3","pages":"231-240"},"PeriodicalIF":5.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10293361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9709905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Correction to: Picking up speed: cell cycle regulation during effector CD8+ T cell differentiation. 校正:拾取速度:效应CD8+ T细胞分化过程中的细胞周期调节。
IF 5.4 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-06-01 DOI: 10.1007/s00430-023-00772-x
Lorenz Kretschmer, Noémie Fuchs, Dirk H Busch, Veit R Buchholz
{"title":"Correction to: Picking up speed: cell cycle regulation during effector CD8<sup>+</sup> T cell differentiation.","authors":"Lorenz Kretschmer,&nbsp;Noémie Fuchs,&nbsp;Dirk H Busch,&nbsp;Veit R Buchholz","doi":"10.1007/s00430-023-00772-x","DOIUrl":"https://doi.org/10.1007/s00430-023-00772-x","url":null,"abstract":"","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 3","pages":"261-262"},"PeriodicalIF":5.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10293326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9712534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Trimer stability of Helicobacter pylori HtrA is regulated by a natural mutation in the protease domain. 幽门螺杆菌HtrA的三聚体稳定性受蛋白酶结构域的自然突变调节。
IF 5.4 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-06-01 DOI: 10.1007/s00430-023-00766-9
Urszula Zarzecka, Nicole Tegtmeyer, Heinrich Sticht, Steffen Backert
{"title":"Trimer stability of Helicobacter pylori HtrA is regulated by a natural mutation in the protease domain.","authors":"Urszula Zarzecka,&nbsp;Nicole Tegtmeyer,&nbsp;Heinrich Sticht,&nbsp;Steffen Backert","doi":"10.1007/s00430-023-00766-9","DOIUrl":"https://doi.org/10.1007/s00430-023-00766-9","url":null,"abstract":"<p><p>The human pathogen Helicobacter pylori is a major risk factor for gastric disease development. Serine protease HtrA is an important bacterial virulence factor that cleaves the cell junction proteins occludin, claudin-8 and E-cadherin, which causes gastric tissue damage. Using casein zymography, we discovered that HtrA trimer stability varies in clinical H. pylori strains. Subsequent sequence analyses revealed that HtrA trimer stability correlated with the presence of leucine or serine residue at position 171. The importance of these amino acids in determining trimer stability was confirmed by leucine-to-serine swapping experiments using isogenic H. pylori mutant strains as well as recombinant HtrA proteins. In addition, this sequence position displays a high sequence variability among various bacterial species, but generally exhibits a preference for hydrophilic amino acids. This natural L/S171 polymorphism in H. pylori may affect the protease activity of HtrA during infection, which could be of clinical importance and may determine gastric disease development.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 3","pages":"241-252"},"PeriodicalIF":5.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10293373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9706112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Functional cross-species conservation of guanylate-binding proteins in innate immunity. 先天性免疫中鸟苷酸结合蛋白的跨物种功能保护。
IF 5.5 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-04-01 Epub Date: 2022-04-13 DOI: 10.1007/s00430-022-00736-7
Luca Schelle, João Vasco Côrte-Real, Pedro José Esteves, Joana Abrantes, Hanna-Mari Baldauf
{"title":"Functional cross-species conservation of guanylate-binding proteins in innate immunity.","authors":"Luca Schelle, João Vasco Côrte-Real, Pedro José Esteves, Joana Abrantes, Hanna-Mari Baldauf","doi":"10.1007/s00430-022-00736-7","DOIUrl":"10.1007/s00430-022-00736-7","url":null,"abstract":"<p><p>Guanylate binding proteins (GBPs) represent an evolutionary ancient protein family widely distributed among eukaryotes. They are interferon (IFN)-inducible guanosine triphosphatases that belong to the dynamin superfamily. GBPs are known to have a major role in the cell-autonomous innate immune response against bacterial, parasitic and viral infections and are also involved in inflammasome activation. Evolutionary studies depicted that GBPs present a pattern of gain and loss of genes in each family with several genes pseudogenized and some genes more divergent, indicative for the birth-and-death evolution process. Most species harbor large GBP gene clusters encoding multiple paralogs. Previous functional studies mainly focused on mouse and human GBPs, but more data are becoming available, broadening the understanding of this multifunctional protein family. In this review, we will provide new insights and give a broad overview about GBP evolution, conservation and their roles in all studied species, including plants, invertebrates and vertebrates, revealing how far the described features of GBPs can be transferred to other species.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 2","pages":"141-152"},"PeriodicalIF":5.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9005921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9276527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immune complexes as culprits of immunopathology in severe COVID-19. 免疫复合物是严重 COVID-19 免疫病理的罪魁祸首。
IF 5.5 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-04-01 Epub Date: 2022-07-23 DOI: 10.1007/s00430-022-00743-8
Philipp Kolb, Sebastian Giese, Reinhard Edmund Voll, Hartmut Hengel, Valeria Falcone
{"title":"Immune complexes as culprits of immunopathology in severe COVID-19.","authors":"Philipp Kolb, Sebastian Giese, Reinhard Edmund Voll, Hartmut Hengel, Valeria Falcone","doi":"10.1007/s00430-022-00743-8","DOIUrl":"10.1007/s00430-022-00743-8","url":null,"abstract":"<p><p>Infection with the pandemic human coronavirus SARS-CoV-2 elicits a respiratory tract disease, termed Coronavirus disease 2019 (COVID-19). While a variable degree of disease-associated symptoms may emerge, severe COVID-19 is commonly associated with respiratory complications such as acute respiratory distress syndrome (ARDS), the necessity for mechanical ventilation or even extracorporeal membrane oxygenation (ECMO). Amongst others, disease outcome depends on age and pre-existing conditions like cardiovascular diseases, metabolic disorders but also age and biological sex. Intriguingly, increasing experimental and clinical evidence suggests that an exacerbated inflammatory response and in particular IgG immune complexes (ICs), significantly contribute to severe and prolonged COVID-19 disease progression. Vast amounts of deposited, unresolved ICs in tissue are capable to initiate an exaggerated Fc gamma receptor (FcγR) mediated signalling cascade which eventually results in common IC-associated organ diseases such as vasculitis, glomerulonephritis and arthritis, comorbidities that have been frequently reported for COVID-19. Moreover and independent of deposited ICs, very recent work identified soluble ICs (sIC) to be also present in the circulation of a majority of severely ill patients, where their systemic abundance correlated with disease severity. Thus, detection of circulating sICs in patients represents a potential marker for critical COVID-19 disease progression. Their detection early after clinical deterioration might become an indicator for the requirement of prompt anti-inflammatory treatment. Here, we review the role of ICs in COVID-19 progression, their possible origins and potential intervention strategies.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 2","pages":"185-191"},"PeriodicalIF":5.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9308473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9646996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
HIV-1 restriction by SERINC5. SERINC5 对 HIV-1 的限制。
IF 5.5 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-04-01 Epub Date: 2022-03-25 DOI: 10.1007/s00430-022-00732-x
Lucía Cano-Ortiz, Tom Luedde, Carsten Münk
{"title":"HIV-1 restriction by SERINC5.","authors":"Lucía Cano-Ortiz, Tom Luedde, Carsten Münk","doi":"10.1007/s00430-022-00732-x","DOIUrl":"10.1007/s00430-022-00732-x","url":null,"abstract":"<p><p>Serine incorporator 5 (SERINC5 or SER5) is a multipass transmembrane protein with ill-defined cellular activities. SER5 was recently described as a human immunodeficiency virus 1 (HIV-1) restriction factor capable of inhibiting HIV-1 that does not express its accessory protein Nef (Δ Nef). SER5 incorporated into the viral membrane impairs the entry of HIV-1 by disrupting the fusion between the viral and the plasma membrane after envelope receptor interaction induced the first steps of the fusion process. The mechanisms of how SER5 prevents membrane fusion are not fully understood and viral envelope proteins were identified that escape the SER5-mediated restriction. Primate lentiviruses, such as HIV-1 and simian immunodeficiency viruses (SIVs), use their accessory protein Nef to downregulate SER5 from the plasma membrane by inducing an endocytic pathway. In addition to being directly antiviral, recent data suggest that SER5 is an important adapter protein in innate signaling pathways leading to the induction of inflammatory cytokines. This review discusses the current knowledge about HIV-1 restriction by SER5.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 2","pages":"133-140"},"PeriodicalIF":5.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10085909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9639539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Interferon antagonists encoded by SARS-CoV-2 at a glance. SARS-CoV-2 编码的干扰素拮抗剂一览。
IF 5.5 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-04-01 Epub Date: 2022-04-02 DOI: 10.1007/s00430-022-00734-9
Jung-Hyun Lee, Lennart Koepke, Frank Kirchhoff, Konstantin M J Sparrer
{"title":"Interferon antagonists encoded by SARS-CoV-2 at a glance.","authors":"Jung-Hyun Lee, Lennart Koepke, Frank Kirchhoff, Konstantin M J Sparrer","doi":"10.1007/s00430-022-00734-9","DOIUrl":"10.1007/s00430-022-00734-9","url":null,"abstract":"<p><p>The innate immune system is a powerful barrier against invading pathogens. Interferons (IFNs) are a major part of the cytokine-mediated anti-viral innate immune response. After recognition of a pathogen by immune sensors, signaling cascades are activated that culminate in the release of IFNs. These activate cells in an autocrine or paracrine fashion eventually setting cells in an anti-viral state via upregulation of hundreds of interferon-stimulated genes (ISGs). To evade the anti-viral effect of the IFN system, successful viruses like the pandemic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evolved strategies to counteract both IFN induction and signaling. In fact, more than half of the about 30 proteins encoded by SARS-CoV-2 target the IFN system at multiple levels to escape IFN-mediated restriction. Here, we review recent insights into the molecular mechanisms used by SARS-CoV-2 proteins to suppress IFN production and the establishment of an anti-viral state.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 2","pages":"125-131"},"PeriodicalIF":5.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8976456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9277972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mouse models in COVID-19 research: analyzing the adaptive immune response. 新冠肺炎研究中的小鼠模型:分析适应性免疫反应。
IF 5.5 3区 医学
Medical Microbiology and Immunology Pub Date : 2023-04-01 Epub Date: 2022-06-04 DOI: 10.1007/s00430-022-00735-8
Sabrina Clever, Asisa Volz
{"title":"Mouse models in COVID-19 research: analyzing the adaptive immune response.","authors":"Sabrina Clever, Asisa Volz","doi":"10.1007/s00430-022-00735-8","DOIUrl":"10.1007/s00430-022-00735-8","url":null,"abstract":"<p><p>The emergence of SARS-CoV-2, the severe acute respiratory syndrome coronavirus type 2 causing the COVID-19 pandemic, resulted in a major necessity for scientific countermeasures. Investigations revealing the exact mechanisms of the SARS-CoV-2 pathogenesis provide the basis for the development of therapeutic measures and protective vaccines against COVID-19. Animal models are inevitable for infection and pre-clinical vaccination studies as well as therapeutic testing. A well-suited animal model, mimicking the pathology seen in human COVID-19 patients, is an important basis for these investigations. Several animal models were already used during SARS-CoV-2 studies with different clinical outcomes after SARS-CoV-2 infection. Here, we give an overview of different animal models used in SARS-CoV-2 infection studies with a focus on the mouse model. Mice provide a well-established animal model for laboratory use and several different mouse models have been generated and are being used in SARS-CoV-2 studies. Furthermore, the analysis of SARS-CoV-2-specific T cells during infection and in vaccination studies in mice is highlighted.</p>","PeriodicalId":18369,"journal":{"name":"Medical Microbiology and Immunology","volume":"212 2","pages":"165-183"},"PeriodicalIF":5.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9166226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9283038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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