Cross-reactive cellular, but not humoral, immunity is detected between OC43 and SARS-CoV-2 NPs in people not infected with SARS-CoV-2: Possible role of cTFH cells

García‐Jiménez, Álvaro Fernando; Cáceres‐Martell, Yaiza; Fernández‐Soto, Daniel; Fleta, Pedro Martínez; Casasnovas, José M.; Sánchez‐Madrid, Francisco; Frade, José Miguel Rodríguez; Valés‐Gómez, Mar; Reyburn, Hugh

doi:10.1002/jlb.4covcra0721-356rrr

Cited by 7 publications

(3 citation statements)

References 32 publications

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“…Humoral immune responses from previous infections might also display cross-reactivity against SARS-CoV-2. SARS-CoV-2 cross-reacting antibodies have been detected in several [ 704 , 705 , 706 , 707 ], but not all [ 708 , 709 , 710 ] studies that analyzed sera obtained or intravenous immunoglobulin manufactured before the pandemic. Some studies found cross-reactive antibodies in only a small percentage of individuals [ 27 , 28 ], implying that genuine variability might have existed within or between populations, possibly related to differences in infection history.…”

Section: Host Factorsmentioning

confidence: 99%

Risk Factors of Severe COVID-19: A Review of Host, Viral and Environmental Factors

Zsichla

Müller

2023

Viruses

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The clinical course and outcome of COVID-19 are highly variable, ranging from asymptomatic infections to severe disease and death. Understanding the risk factors of severe COVID-19 is relevant both in the clinical setting and at the epidemiological level. Here, we provide an overview of host, viral and environmental factors that have been shown or (in some cases) hypothesized to be associated with severe clinical outcomes. The factors considered in detail include the age and frailty, genetic polymorphisms, biological sex (and pregnancy), co- and superinfections, non-communicable comorbidities, immunological history, microbiota, and lifestyle of the patient; viral genetic variation and infecting dose; socioeconomic factors; and air pollution. For each category, we compile (sometimes conflicting) evidence for the association of the factor with COVID-19 outcomes (including the strength of the effect) and outline possible action mechanisms. We also discuss the complex interactions between the various risk factors.

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Section: Host Factorsmentioning

confidence: 99%

Risk Factors of Severe COVID-19: A Review of Host, Viral and Environmental Factors

Zsichla

Müller

2023

Viruses

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“…In the peripheral blood, a subset of CD4 + T-cells with a similar phenotype and function has been described, termed circulating T FH cells (cT FH ) [21]. In COVID-19, cT FH have been proposed to play a crucial role in antiviral immunity [22]. SARS-CoV-2-specific cT FH are expanded in convalescent individuals, and are associated with antibody titers [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

High and Sustained Ex Vivo Frequency but Altered Phenotype of SARS-CoV-2-Specific CD4+ T-Cells in an Anti-CD20-Treated Patient with Prolonged COVID-19

Cords

Knapp

Woost

et al. 2022

Viruses

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Here, we longitudinally assessed the ex vivo frequency and phenotype of SARS-CoV-2 membrane protein (aa145–164) epitope-specific CD4+ T-cells of an anti-CD20-treated patient with prolonged viral positivity in direct comparison to an immunocompetent patient through an MHC class II DRB1*11:01 Tetramer analysis. We detected a high and stable SARS-CoV-2 membrane-specific CD4+ T-cell response in both patients, with higher frequencies of virus-specific CD4+ T-cells in the B-cell-depleted patient. However, we found an altered virus-specific CD4+ T-cell memory phenotype in the B-cell-depleted patient that was skewed towards late differentiated memory T-cells, as well as reduced frequencies of SARS-CoV-2-specific CD4+ T-cells with CD45RA− CXCR5+ PD-1+ circulating T follicular helper cell (cTFH) phenotype. Furthermore, we observed a delayed contraction of CD127− virus-specific effector cells. The expression of the co-inhibitory receptors TIGIT and LAG-3 fluctuated on the virus-specific CD4+ T-cells of the patient, but were associated with the inflammation markers IL-6 and CRP. Our findings indicate that, despite B-cell depletion and a lack of B-cell—T-cell interaction, a robust virus-specific CD4+ T-cell response can be primed that helps to control the viral replication, but which is not sufficient to fully abrogate the infection.

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“…At least, several types of cross-reactive CD8 + T cells and type 1 helper T cell (Th1) CD4 + T cells that support CTL functions [ 67 , 73 ] can influence disease severity and outcome [ 74 , 75 ]. The importance of cross-reactive, CD4 + follicular helper T (Tfh) cells that support antibody production remains to be determined [ 76 , 77 ].…”

Section: Introductionmentioning

confidence: 99%

Association of cellular immunity with severity of COVID-19 from the perspective of antigen-specific memory T cell responses and cross-reactivity

et al. 2022

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Coronaviruses regularly cause outbreaks of zoonotic diseases characterized by severe pneumonia. The new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused the global pandemic disease COVID-19 that began at the end of 2019 and spread rapidly owing to its infectious nature and rapidly progressing pneumonia. Although the infectivity of SARS-CoV-2 is high, indicated by the worldwide spread of the disease in a very short period, many individuals displayed only subclinical infection, and some of them transmitted the disease to individuals who then developed a severe symptomatic infection. Furthermore, there are differences in the severity of infection across countries, which can be attributed to factors such as the emergence of viral mutations in a short period of time as well as to the immune responses to viral factors. Anti-viral immunity generally consists of neutralizing antibodies that block viral infection and cytotoxic CD8+ T cells that eliminate the virus-infected cells. There is compelling evidence for the role of neutralizing antibodies in protective immunity in SARS-CoV-2 infection. However, the role of CD4+ and CD8+ T cells after the viral entry is complex and warrants a comprehensive discussion. Here, we discuss the protection afforded by cellular immunity against initial infection and development of severe disease. The initial failure of cellular immunity to control the infection worsens the clinical outcomes and functional profiles that inflict tissue damage without effectively eliminating viral reservoirs, while robust T cell responses are associated with mild outcomes. We also discuss persistent long-lasting memory T cell-mediated protection after infection or vaccination, which is rather complicated as it may involve SARS-CoV-2-specific cytotoxic T lymphocytes or cross-reactivity with previously infected seasonal coronaviruses, which are largely related to HLA genotypes. In addition, cross-reactivity with mutant strains is also discussed. Lastly, we discuss appropriate measures to be taken against the disease for immunocompromised patients. In conclusion, we provide evidence and discuss the causal relationship between natural infection- or vaccine-mediated memory T cell immunity and severity of COVID-19. This review is expected to provide a basis to develop strategies for the next generation of T cell-focused vaccines and aid in ending the current pandemic.

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Cross-reactive cellular, but not humoral, immunity is detected between OC43 and SARS-CoV-2 NPs in people not infected with SARS-CoV-2: Possible role of cTFH cells

Cited by 7 publications

References 32 publications

Risk Factors of Severe COVID-19: A Review of Host, Viral and Environmental Factors

Risk Factors of Severe COVID-19: A Review of Host, Viral and Environmental Factors

High and Sustained Ex Vivo Frequency but Altered Phenotype of SARS-CoV-2-Specific CD4+ T-Cells in an Anti-CD20-Treated Patient with Prolonged COVID-19

Association of cellular immunity with severity of COVID-19 from the perspective of antigen-specific memory T cell responses and cross-reactivity

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