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Source: COVID-19 Research  Jul 30, 2021  2 years ago
British And American Researchers Finds That The Bacteria Streptococcus Pneumoniae Modulates Human Host Immunity To SARS-CoV-2 Virus
British And American Researchers Finds That The Bacteria Streptococcus Pneumoniae Modulates Human Host Immunity To SARS-CoV-2 Virus
Source: COVID-19 Research  Jul 30, 2021  2 years ago
Researchers from Liverpool School of Tropical Medicine-UK, Liverpool University Hospitals –UK, University of Oxford-UK and Pfizer Vaccines-USA in a new study investigating the immunological consequences of secondary Streptococcus pneumoniae (S. pneumoniae) infection in COVID-19 patients have found that S. pneumoniae, which is a Gram-positive bacterium responsible for pneumonia, modulates the host immune system to facilitate the immune escape of the SARS-CoV-2 coronavirus.

Despite the fact that recent epidemiological data suggest that pneumococci may contribute to the risk of SARS-CoV-2 disease, secondary pneumococcal pneumonia has been reported as infrequent.
This apparent contradiction may be explained by interactions of SARS-CoV-2 and pneumococcus in the upper airway, resulting in the escape of SARS-CoV-2 from protective host immune responses.
The study team investigated the relationship of these two respiratory pathogens in two distinct cohorts of a) healthcare workers with asymptomatic or mildly symptomatic SARS-CoV-2 infection identified by systematic screening and b) patients with moderate to severe disease who presented to hospital.
The team assessed the effect of co-infection on host antibody, cellular and inflammatory responses to the virus. In both cohorts, pneumococcal colonisation was associated with diminished anti-viral immune responses, which affected primarily mucosal IgA levels among individuals with mild or asymptomatic infection and cellular memory responses in infected patients.
The study findings suggest that S. pneumoniae modulates host immunity to SARS-CoV-2 and raises the question as to whether the pneumococcal carriage also enables immune escape of other respiratory viruses through a similar mechanism and facilitates reinfection occurrence.
The study findings were published on a preprint server and are currently being peer reviewed.
The bacterial colonization in the upper respiratory tract is considered to be one of the major risk factors of COVID-19.
In this context, studies have shown that the co-occurrence of invasive pneumococcal disease in COVID-19 patients increases the risk of mortality.
Typically, an interaction between S. pneumoniae and respiratory viruses, such as influenza virus and respiratory syncytial virus, in the upper respiratory tract increases the risk of secondary pneumococcal pneumonia.
However, in COVID-19 patients, the incidence of pneumococcal pneumonia has been observed only rarely. This could be due to low bacterial transmission owing to non-pharmacological control measures or low bacterial detection because of excessive use of empiric antibiotics.    
Interestingly from the immunological perspective, studies have shown that during viral infection, bacterial colocalization in the upper respiratory tract can lead to modulation of host immune responses, which in turn can facilitate immune evasion of the virus.
The study team investigated the impact of S. pneumoniae and SARS-CoV-2 co-infection on host adaptive immune responses.
The clinical research was conducted on healthcare workers with a symptomatic or mildly symptomatic COVID-19 and hospitalized COVID-19 patients with moderate-to-severe disease.
In both groups, the study team estimated the prevalence of S. pneumoniae and SARS-CoV-2 co-infection and its impact on COVID-19 severity, immune responses, and inflammation.
Out of 85 enrolled healthcare workers, 29 tested positive for SARS-CoV-2 and 17 tested positive for S. pneumoniae. The prevalence of S. pneumoniae infection was significantly higher in SARS-CoV-2 positive participants than SARS-CoV-2 negative participants.
In the other group,  out of 400 enrolled hospitalized patients, 255 tested positive for SARS-CoV-2 and 35 tested positive for S. pneumoniae. However, no significant difference in S. pneumoniae prevalence was observed between SARS-CoV-2 positive and negative patients.
Importantly, no effect of S. pneumoniae co-infection on upper airway viral load and disease severity was observed among participants.
As the SARS-CoV-2 virus primarily attacks upper airway epithelial cells, IgA antibody-induced mucosal antiviral immunity is expected to play a vital role in the early elimination of the virus.
In order to characterize mucosal immune responses, the study team measured the levels of IgA-specific anti-SARS-CoV-2 antibodies in saliva and nasal samples.
The study findings revealed that in SARS-CoV-2 positive healthcare workers, S. pneumoniae co-infection led to a significant reduction in mucosal IgA responses to SARS-CoV2.
However, in SARS-CoV-2 positive hospitalized patients, this change was not very prominent. Regarding systemic antibody responses, SARS-CoV-2 positive healthcare workers with S. pneumoniae co-infection showed a trend toward lower induction of IgG-specific immune responses to SARS-CoV-2. However, in hospitalized patients with S. pneumoniae co-infection, significantly lower levels of IgG-specific anti-SARS-CoV-2 antibodies were detected in serum samples.
In addition, for mechanistic evaluation, the study team conducted a series of co-colonization experiments with live-attenuated influenza virus and S. pneumoniae.
The study findings revealed that S. pneumoniae infection occurred prior to influenza virus exposure led to suppression of IgA immune responses to influenza virus. In contrast, no such alteration was observed when viral exposure occurred before S. pneumoniae infection.
In order to evaluate long-term humoral immunity, the scientists isolated SARS-CoV-2 specific memory B cells from peripheral blood mononuclear cells of participants.
The study findings revealed that co-infection with S. pneumoniae and SARS-CoV-2 resulted in reduced memory B cell response to SARS-CoV-2 antigens in both healthcare workers and patients.
Also in hospitalized patients co-infected with S. pneumoniae, significantly lower levels of CD4+ T cell response to SARS-CoV-2 spike, nucleocapsid, and S1 antigens were observed. A similar trend was observed for CD8+ T cell responses to different SARS-CoV-2 antigens.  
The study team measured the levels of 30 cytokines in nasal and serum samples during acute infection to investigate SARS-CoV-2 induced inflammatory responses.
The clinical findings revealed that in hospitalized patients, S. pneumoniae co-infection resulted in a reduced serum inflammatory profile.
However, in both colonized and non-colonized healthcare workers, the level of inflammation was lower than in hospitalized patients.
Interestingly in nasal samples, healthcare workers showed reduced levels of certain cytokines that are associated with T cell maturation and differentiation.
In both healthcare workers and hospitalized patients, S. pneumoniae infection did not cause a variation in cytokines associated with T cell proliferation and activation.
The research findings highlight the significance of S. pneumoniae infection in COVID-19 patients in modulating host adaptive immunity against SARS-CoV-2, which in turn can facilitate viral immune evasion. As mentioned by the study team, colocalization of S. pneumoniae with SARS-CoV-2 may increase the risk of long-COVID or SARS-CoV-2 reinfection.
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