To determine risk for avian influenza virus infection, we conducted serologic surveillance for H5 and H9 subtypes among poultry workers in Beijing, China, 2009–2010, and assessed workers’ understanding of avian influenza. We found that poultry workers had considerable risk for infection with H9 subtypes. Increasing their knowledge could prevent future infections.
As a respiratory tract virus, SARS-CoV-2 infected people through contacting with the upper respiratory tract first. Previous studies indicated that microbiota could modulate immune response against pathogen infection. In the present study, we performed metagenomic sequencing of pharyngeal swabs from eleven patients with COVID-19 and eleven Non-COVID-19 patients who had similar symptoms such as fever and cough. Through metagenomic analysis of the above two groups and a healthy group from the public data, there are 6502 species identified in the samples. Specifically, the Pielou index indicated a lower evenness of the microbiota in the COVID-19 group than that in the Non-COVID-19 group. Combined with the linear discriminant analysis (LDA) and the generalized linear model, eighty-one bacterial species were found with increased abundance in the COVID-19 group, where 51 species were enriched more than 8 folds. The top three enriched genera were
Streptococcus
,
Prevotella
and
Campylobacter
containing some opportunistic pathogens. More interestingly, through experiments, we found that two
Streptococcus
strains,
S. suis
and
S. agalactiae
, could stimulate the expression of ACE2 of Vero cells
in vitro
, which may promote SARS-CoV-2 infection. Therefore, these enriched pathogens in the pharynxes of COVID-19 patients may involve in the virus-host interactions to affect SARS-CoV-2 infection and cause potential secondary bacterial infections through changing the expression of the viral receptor ACE2 and/or modulate the host’s immune system.
Supplementary Information
The online version contains supplementary material available at 10.1007/s12250-021-00391-x.
Tuberculosis (TB), caused by
Mycobacterium tuberculosis
(
M. tuberculosis
), is one of the most fatal diseases in the world. Methylenetetrahydrofolate reductase (MTHFR) catalyzes the production of 5-methyltetrahydrofolate (5-CH
3
-THF), which is required for the
de novo
biosynthesis of methionine in bacteria. In this study, we identified Rv2172c as an MTHFR in
M. tuberculosis
through
in vitro
and
in vivo
analyses and determined that the protein was essential for the
in vitro
growth of the bacterium. Subsequently, we constructed
rv2172c
R159N and L214A mutants in
M. tuberculosis
, and found that these mutants were more sensitive to the antifolates
para
-aminosalicylic acid (PAS) and sulfamethoxazole (SMX). Combining biochemical and genetic methods, we found that
rv2172c
R159N or L214A mutation impaired methionine production, leading to increased susceptibility of
M. tuberculosis
to PAS, which was largely restored by adding exogenous methionine. Moreover, overexpression of
rv2172c
in
M. tuberculosis
could increase methionine production and lead to PAS resistance. This research was the first to identify an MTHFR in
M.
tuberculosis
and revealed that the activity of this enzyme was associated with susceptibility to antifolates. These findings have particular value for anti-tubercular drugs design for the treatment of drug-resistant TB.
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