Immunity and immunopathology to viruses: what decides the outcome?

Rouse, Barry T.; Sehrawat, Sharvan

doi:10.1038/nri2802

Cited by 486 publications

(436 citation statements)

References 139 publications

Supporting

Mentioning

428

Contrasting

Unclassified

Order By: Relevance

“…However, approximately 85% of patients respond with IL-10-producing CD8+ and CD4+ T cells, and occasionally FoxP3+ T regs (Wang J-P, 2010). These patients develop chronic HCV infection, while those that respond with a Th1 response clear the virus (Rouse BT, 2010). Hall et al showed that HCV-infected hepatocytes are capable of inducing T regs .…”

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

“…IL-10 can also inhibit pro-inflammatory cytokine signaling pathways such as NF-κB. In addition, IL-10 suppresses phosphorylation of STAT1 and induces suppressor of cytokine signaling 3 (SOCS3) expression by neutrophils and macrophages (Rouse BT, 2010). Protective immunity against hepatitis C virus is associated with a robust Th1 response and production of IFN-.…”

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

“…However, some viruses have exploited the regulatory immune response, and trigger T reg activation early in the course of disease, leading to immune suppression and viral persistence. Viruses activate endosomal TLRs 3, 7, 8, and 9 (Rouse BT, 2010). Of those, only TLR 7, 8, and 9 are expressed in T regs .…”

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

“…In addition, when these infected DCs are cultured with allogenic T cells, they also expanded the population of regulatory T cells (Cao S, 2011). Dendritic cells from lymphocytic choriomeningitis virus-infected mice and monocytes from people infected with hepatitis B, hepatitis C, and human immunodeficiency virus similarly produce increased levels of IL-10 (reviewed in (Rouse BT, 2010)). IL-10 blocks production of pro-inflammatory cytokines and chemokines, and down-regulates MHC class II expression.…”

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

See 3 more Smart Citations

Regulatory T Cells and Viral Disease

LeRoith¹,

Ahmed²

2012

Inflammation, Chronic Diseases and Cancer - Cell and Molecular Biology, Immunology and Clinical Bases

View full text Add to dashboard Cite

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

Section: Viral-mediated Regulatory T Cell Inductionmentioning

confidence: 99%

See 2 more Smart Citations

Regulatory T Cells and Viral Disease

LeRoith¹,

Ahmed²

2012

Inflammation, Chronic Diseases and Cancer - Cell and Molecular Biology, Immunology and Clinical Bases

View full text Add to dashboard Cite

“…HCV successfully evades the immune response in 60% -80% of cases, resulting in chronic liver disease. Conversely, the immune response to HAV is robust and extremely effective in eliminating the virus and results in a naturally acute disease that in most cases resolves spontaneously [6,7].…”

Section: Introductionmentioning

confidence: 99%

Rethinking cytokine function during hepatitis A and hepatitis C infections

Fierro¹,

Castro-García²,

Panduro³

2013

ABB

View full text Add to dashboard Cite

Hepatitis A virus (HAV) and hepatitis C virus (HCV) are both viruses with hepatotropic lifestyles. HAV induces an acute infection that results in the elimination of the virus by the host whereas HCV is typically able to establish a persistent infection that may result in cirrhosis and hepatocellular carcinoma. The mechanisms responsible for this difference are unknown. However, given HAV and HCV are both non-cytophatic viruses, the observed symptoms and liver injury during the infections are the result of specific immune responses under the control of cytokines. Thus, the production of cytokines during hepatotropic viral infections may constitute a mechanism leading to different outcomes. Therefore, understanding the differences in the cytokine patterns induced in response to HAV and HCV is likely to provide important insights into the cytokine-mediated mechanisms underlying the long-term persistence of HCV, the broad spectrum of clinical manifestations induced by HAV and the resolution of HAV infection during the acute phase. Herein, we focus on discoveries that hold promise in identifying cytokines as therapeutic targets for the treatment of viral hepatitis.

show abstract

Estimation of the Timing and Intensity of Reemergence of Respiratory Syncytial Virus Following the COVID-19 Pandemic in the US

Zheng¹,

Pitzer²,

Shapiro

et al. 2021

JAMA Netw Open

View full text Add to dashboard Cite

IMPORTANCERespiratory syncytial virus (RSV) is a leading cause of hospitalizations in young children. RSV largely disappeared in 2020 owing to precautions taken because of the COVID-19 pandemic. Estimating the timing and intensity of the reemergence of RSV and the age groups affected is crucial for planning for the administration of prophylactic antibodies and anticipating hospital capacity. OBJECTIVE To examine the association of different factors, including mitigation strategies, duration of maternal-derived immunity, and importation of external infections, with the dynamics of reemergent RSV epidemics. DESIGN, SETTING, AND PARTICIPANTS This simulation modeling study used mathematical models to reproduce the annual epidemics of RSV before the COVID-19 pandemic in New York and California.These models were modified to project the trajectory of RSV epidemics from 2020 to 2025 under different scenarios with varying stringency of mitigation measures for SARS-CoV-2. Simulations also evaluated factors likely to affect the reemergence of RSV epidemics, including introduction of the virus from out-of-state sources and decreased transplacentally acquired immunity in infants. Models using parameters fitted to similar inpatient data sets from Colorado and Florida were used to illustrate these associations in populations with biennial RSV epidemics and year-round RSV circulation, respectively. Statistical analysis was performed from February to October 2021. MAIN OUTCOMES AND MEASURESThe primary outcome of this study was defined as the estimated number of RSV hospitalizations each month in the entire population. Secondary outcomes included the age distribution of hospitalizations among children less than 5 years of age, incidence of any RSV infection, and incidence of RSV lower respiratory tract infection. RESULTS Among a simulated population of 19.45 million people, virus introduction from external sources was associated with the emergence of the spring and summer epidemic in 2021. There was a tradeoff between the intensity of the spring and summer epidemic in 2021 and the intensity of the epidemic in the subsequent winter. Among children 1 year of age, the estimated incidence of RSV hospitalizations was 707 per 100 000 children per year in the 2021 and 2022 RSV season, compared with 355 per 100 000 children per year in a typical RSV season. CONCLUSIONS AND RELEVANCEThis simulation modeling study found that virus introduction from external sources was associated with the spring and summer epidemics in 2021. These findings suggest that pediatric departments should be alert to large RSV outbreaks in the coming seasons, the intensity of which could depend on the size of the spring and summer epidemic in that location.Enhanced surveillance is recommended for both prophylaxis administration and hospital capacity management.

show abstract

Immunity and immunopathology to viruses: what decides the outcome?

Cited by 486 publications

References 139 publications

Regulatory T Cells and Viral Disease

Regulatory T Cells and Viral Disease

Rethinking cytokine function during hepatitis A and hepatitis C infections

Estimation of the Timing and Intensity of Reemergence of Respiratory Syncytial Virus Following the COVID-19 Pandemic in the US

Contact Info

Product

Resources

About