Respiratory syncytial virus: immunopathology and control

Zhang, Weidong; Lockey, Richard F.; Mohapatra, Shyam S.

doi:10.1586/1744666x.2.1.169

Cited by 5 publications

(6 citation statements)

References 112 publications

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“…RSV, a member of the Paramyxoviridae family, is the primary and repeat infections being responsible for a range of illnesses, from common cold-like symptoms to serious lower respiratory tract diseases including bronchiolitis (Zhang et al, 2006;Villenave et al, 2013). RSV infectionrelated illnesses and its mechanism have not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…TLRs family are a type of pattern recognition receptors, which are considered to be the first line of innate defense (Kim and Lee, 2014). The primary target for RSV in humans is airway respiratory epithelial cells and the first link of defense against the virus involves epithelial production of a plethora of cytokines, chemokines, and immune modulatory mediators (Krishnan et al, 2004;Zhang and Lockey, 2006). Early studies have indicated that TLRs 1-6 are expressed in human bronchial epithelium (Becker et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

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Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b

Liu

Gao

Wang

et al. 2015

Cell Biology International

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Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract illnesses in infants worldwide. TLR4 signal pathway plays a critical role in regulating immune response against RSV infection. However, the activation of TLR4 in RSV infection is still unclear. In present study, the expression levels of miR-26b and TLR4 mRNA were detected in peripheral blood mononuclear cells (PBMCs) of children with or without RSV infected bronchiolitis. The expression levels of TLR4 and its downstream genes IFNβ and CCL5 were also quantified in PBMCs infected with RSVΔG or RSV A2 in vitro. The results showed that children with RSV infection had higher miR-26b level and lower TLR4 mRNA level in PBMCs. miR-26b was predicted to target TLR4. In vitro, miR-26b mimic markedly down-regulated TLR4 mRNA/protein expression and IFNβ/CCL5 concentrations while miR-26b inhibitor up-regulated these levels. This study reveals that RSV infection inhibits TLR4 signaling via up-regulation of miR-26b, which provides a potential therapeutic target for preventing and treating RSV infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b

Liu

Gao

Wang

et al. 2015

Cell Biology International

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“…Of interest, RSV does not induce robust, long term immunity and people may be repeatedly infected with the same and different strains of RSV (55, 56). These finding are particularly relevant to the multiple failed RSV vaccine trails to date, including the original formalin inactivated RSV (FI-RSV) vaccine as well as more recent subunit and live attenuated vaccines.…”

Section: Introductionmentioning

confidence: 99%

Role of Type I Interferon (IFN) in the Respiratory Syncytial Virus (RSV) Immune Response and Disease Severity

Hijano

Kauvar

et al. 2019

Front. Immunol.

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Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in children <2 years of age. Increased morbidity and mortality have been reported in high-risk patients, such as premature infants, patients with cardiac disease, and severely immune compromised patients. Severe disease is associated with the virulence of the virus as well as host factors specifically including the innate immune response. The role of type I interferons (IFNs) in the response to RSV infection is important in regulating the rate of virus clearance and in directing the character of the immune response, which is normally associated with protection and less severe disease. Two RSV non-structural proteins, NS1 and NS2, as well as the envelope G glycoprotein are known to suppress type I IFN production and a robust type I IFN response to RSV does not occur in human infants or neonatal mouse models of RSV infection. Additionally, presence of type I IFNs are associated with mild symptoms in infants and administration of IFN-α prior to infection of neonatal mice with RSV reduces immunopathology. This evidence has driven RSV prophylaxis and therapeutic efforts to consider strategies for enhancing type I IFN production.

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“…65 RSV mortality and morbidity increase among infants, the immunocompromised, and pulmonary hypertensive populations. 66,67 Seniors in particular remain at high risk for RSV infections because they may be exposed to nosocomial infections in the hospital or long-term care facilities. 68,69 The most notorious RSV vaccine failure used formalininactivated RSV (FI-RSV) to stimulate immunity, much like the Salk polio vaccine.…”

Section: Etiologic Agents Of Respiratory Tract Infectionsmentioning

confidence: 99%

“…Despite the strong evidence for a link between asthma and respiratory infections, the direction of causality between viral infections and asthma is still heatedly debated. Although there is a growing body of evidence supporting a causal relationship for HRV, a similar relationship for RSV is difficult to prove because virtually all children have been infected with RSV by the age of 2 years 66,79 ; therefore, the development of asthma likely depends on genetic and/or atopic factors. 175 Simõ es and colleagues 176 recently reported new evidence that associates RSV infection with the development of recurrent wheeze in nonatopic infants, in a worldwide, multicenter, 24-month investigation.…”

Section: Challenges and Opportunities For Asthma Therapymentioning

confidence: 99%

The Infectious March: The Complex Interaction Between Microbes and the Immune System in Asthma

Wong

Hellermann

Mohapatra

2010

Immunology and Allergy Clinics of North America

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There has been significant progress in our knowledge about the relationship between infectious disease and the immune system in relation to asthma, but many unanswered questions still remain. Respiratory tract infections such as those caused by respiratory syncytial virus and rhinovirus during the first two years of life are still clearly associated with later wheezing and asthma, but the mechanism has not been completely worked out. Is there an 'infectious march' triggered by infection in infancy that progresses to disease pathology or are infants who contract respiratory infections predisposed to developing asthma? This review focuses on the common themes in the interaction between microbes and the immune system and presents a critical appraisal of the evidence to date. The various mechanisms whereby microbes alter the immune response and how this might influence asthma are discussed along with new and promising clinical practices for prevention and therapy. Recent advances in utilizing sensitive PCR detection methods have allowed more rigorous testing of the causality hypothesis of virus infection leading to asthma, but the evidence is still equivocal. Various exceptions and inconsistencies in the clinical trials are discussed in light of new guidelines for subject inclusion/exclusion in hopes of providing some standardization. In spite of past failures in vaccination and disappointing results of some clinical trials, the new strategies for prophylaxis including RNA interference and targeted delivery of microbicides offer a large dose of hope to a world suffering from an increasing incidence of asthma and a huge burden of healthcare cost and loss of quality of life.

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Respiratory syncytial virus: immunopathology and control

Cited by 5 publications

References 112 publications

Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b

Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b

Role of Type I Interferon (IFN) in the Respiratory Syncytial Virus (RSV) Immune Response and Disease Severity

The Infectious March: The Complex Interaction Between Microbes and the Immune System in Asthma

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