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1.
Crit Rev Immunol ; 40(6): 485-496, 2020.
Article in English | MEDLINE | ID: mdl-33900693

ABSTRACT

In December 2019, outbreak of a novel coronavirus flared in Wuhan, the capital city of Hubei province, China. The identified pathogen was an enveloped RNA betacoronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The outbreak was declared a pandemic by the World Health Organization (WHO), because the continual spread of this deadly and highly infectious virus is a health emergency for all world nations. SARS-CoV-2 is associated with severe atypical pneumonia coronavirus disease-19. Typical symptoms of this disease include fever, malaise, cough, shortness of breath, and in severe cases, death. As the virus continues to invade host cells deep into alveoli, infection severity mostly depends on the undeterred immune response that is triggered by elevated levels of inflammation-inducing cytokines, called a cytokine storm. In this article, we provide a comprehensive review of the viral life cycle and immunological responses associated with the SARS-CoV-2 infection.


Subject(s)
COVID-19/etiology , Disease Susceptibility , Host-Pathogen Interactions/immunology , SARS-CoV-2/physiology , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/therapy , Cytokine Release Syndrome/diagnosis , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/therapy , Disease Susceptibility/immunology , Humans , Immune Evasion , Immunity, Cellular , Immunity, Innate , Severity of Illness Index
2.
Microbiol Resour Announc ; 8(37)2019 Sep 12.
Article in English | MEDLINE | ID: mdl-31515350

ABSTRACT

Lactobacilli are dominant members of the healthy female bladder microbiota. Here, we report the complete genome sequences of six Lactobacillus gasseri and three Lactobacillus paragasseri strains isolated from catheterized urine samples. These L. paragasseri genomes are the first publicly available sequences of the species from the bladder.

3.
PLoS One ; 13(2): e0192606, 2018.
Article in English | MEDLINE | ID: mdl-29447215

ABSTRACT

We investigated maternal obesity in inbred SM/J mice by assigning females to a high-fat diet or a low-fat diet at weaning, mating them to low-fat-fed males, cross-fostering the offspring to low-fat-fed SM/J nurses at birth, and weaning the offspring onto a high-fat or low-fat diet. A maternal high-fat diet exacerbated obesity in the high-fat-fed daughters, causing them to weigh more, have more fat, and have higher serum levels of leptin as adults, accompanied by dozens of gene expression changes and thousands of DNA methylation changes in their livers and hearts. Maternal diet particularly affected genes involved in RNA processing, immune response, and mitochondria. Between one-quarter and one-third of differentially expressed genes contained a differentially methylated region associated with maternal diet. An offspring high-fat diet reduced overall variation in DNA methylation, increased body weight and organ weights, increased long bone lengths and weights, decreased insulin sensitivity, and changed the expression of 3,908 genes in the liver. Although the offspring were more affected by their own diet, their maternal diet had epigenetic effects lasting through adulthood, and in the daughters these effects were accompanied by phenotypic changes relevant to obesity and diabetes.


Subject(s)
DNA Methylation , Diet, High-Fat , Gene Expression , Mothers , Obesity/epidemiology , Animals , Female , Mice , Risk Factors
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