Evidence for Cross-Protection Against Subsequent Febrile Respiratory Illness Episodes From Prior Infections by Different Viruses Among Singapore Military Recruits 2009–2014

Chen, Mark; Loh, Jin Phang; Chuah, Cheryl X P; Gao, Qingbo; Sun, Yan; Ng, Sock Hoon; Koh, Wee-Hong Victor; Goh, Ee Hui; Zhao, Xiahong; Tambyah, Paul Anantharajah; Cook, Alex R.; Chng, Jeremiah; Pang, Junxiong; Tan, Bernard C. Y.; Lee, Vernon J.

doi:10.1093/infdis/jiz046

Cited by 13 publications

(14 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similarly, immune cells and club cells that survived an initial IAV infection nonspecifically mediated protection against an influenza B virus challenge through alterations in the composition of cellular infiltration and inflammatory cytokine profiles; it is possible cells in the lung following the initial RSV infection in this study were similarly primed to protect against the secondary influenza virus challenge (52). Consistent with results in mice, infection with influenza virus or adenovirus has been documented to provide protection against subsequent febrile respiratory illnesses in humans (53). Thus, it is possible that memory T cells and innate immune responses may have contributed nonspecifically to the TRM-mediated protection against IAV infection observed in this study.…”

Section: Discussionsupporting

confidence: 76%

Tissue-Resident Memory T Cells in the Lungs Protect against Acute Respiratory Syncytial Virus Infection

et al. 2021

View full text Add to dashboard Cite

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection in young children. The T cell response plays a critical role in facilitating clearance of an acute RSV infection, and memory T cell responses are vital for protection against secondary RSV exposures. Tissue-resident memory (TRM) T cells have been identified as a subset of memory T cells that reside in nonlymphoid tissues and are critical for providing long-term immunity. There is currently limited information regarding the establishment and longevity of TRM T cell responses elicited following an acute RSV infection as well as their role in protection against repeated RSV infections. In this study, we examined the magnitude, phenotype, and protective capacity of TRM CD4 and CD8 T cells in the lungs of BALB/c mice following an acute RSV infection. TRM CD4 and CD8 T cells were established within the lungs and waned by 149 d following RSV infection. To determine the protective capacity of TRMs, FTY720 administration was used to prevent trafficking of peripheral memory T cells into the lungs prior to challenge of RSV-immune mice, with a recombinant influenza virus expressing either an RSV-derived CD4 or CD8 T cell epitope. We observed enhanced viral clearance in RSV-immune mice, suggesting that TRM CD8 T cells can contribute to protection against a secondary RSV infection. Given the protective capacity of TRMs, future RSV vaccine candidates should focus on the generation of these cell populations within the lung to induce effective immunity against RSV infection. ImmunoHorizons, 2021, 5: 59-69.

show abstract

Section: Discussionsupporting

confidence: 76%

Tissue-Resident Memory T Cells in the Lungs Protect against Acute Respiratory Syncytial Virus Infection

et al. 2021

View full text Add to dashboard Cite

show abstract

“…These observations in 1918 also are supported by more recent examples. Among military recruits in Singapore in 2009–2013, prior adenovirus or influenza virus infection conferred cross-protection against subsequent febrile illness episodes relative to prior infection due to other circulating viruses [34].…”

Section: Discussionmentioning

confidence: 99%

Race and 1918 Influenza Pandemic in the United States: A Review of the Literature

Økland

Mamelund

2019

IJERPH

View full text Add to dashboard Cite

During epidemics, the poorest part of the population usually suffers the most. Alfred Crosby noted that the norm changed during the 1918 influenza pandemic in the US: The black population (which were expected to have higher influenza morbidity and mortality) had lower morbidity and mortality than the white population during the autumn of 1918. Crosby’s explanation for this was that black people were more exposed to a mild spring/summer wave of influenza earlier that same year. In this paper, we review the literature from the pandemic of 1918 to better understand the crossover in the role of race on mortality. The literature has used insurance, military, survey, and routine notification data. Results show that the black population had lower morbidity, and during September, October, and November, lower mortality but higher case fatality than the white population. The results also show that the black population had lower influenza morbidity prior to 1918. The reasons for lower morbidity among the black population both at baseline and during the herald and later waves in 1918 remain unclear. Results may imply that black people had a lower risk of developing the disease given exposure, but when they did get sick, they had a higher risk of dying.

show abstract

“…NK cells are also key mediators of cross-protection whereby they expand during the initial infection and are primed to undergo a second expansion as well as produce more cytokines upon a secondary infection ( 207 ). More recently, a Singapore study of military recruits within a 5-year period showed that men infected with influenza were protected against subsequent infection with adenovirus ( 79 ). It should be noted, however, that cross-protection between infections is generally considered to be dependent on both non-specific reprogramming of innate immunity as well as activation of memory T cells.…”

Section: Toll-like Receptor Agonist-mediated Trained Immunity and Promentioning

confidence: 99%

TLR Agonists as Mediators of Trained Immunity: Mechanistic Insight and Immunotherapeutic Potential to Combat Infection

et al. 2021

View full text Add to dashboard Cite

Despite advances in critical care medicine, infection remains a significant problem that continues to be complicated with the challenge of antibiotic resistance. Immunocompromised patients are highly susceptible to development of severe infection which often progresses to the life-threatening condition of sepsis. Thus, immunotherapies aimed at boosting host immune defenses are highly attractive strategies to ward off infection and protect patients. Recently there has been mounting evidence that activation of the innate immune system can confer long-term functional reprogramming whereby innate leukocytes mount more robust responses upon secondary exposure to a pathogen for more efficient clearance and host protection, termed trained immunity. Toll-like receptor (TLR) agonists are a class of agents which have been shown to trigger the phenomenon of trained immunity through metabolic reprogramming and epigenetic modifications which drive profound augmentation of antimicrobial functions. Immunomodulatory TLR agonists are also highly beneficial as vaccine adjuvants. This review provides an overview on TLR signaling and our current understanding of TLR agonists which show promise as immunotherapeutic agents for combating infection. A brief discussion on our current understanding of underlying mechanisms is also provided. Although an evolving field, TLR agonists hold strong therapeutic potential as immunomodulators and merit further investigation for clinical translation.

show abstract

Evidence for Cross-Protection Against Subsequent Febrile Respiratory Illness Episodes From Prior Infections by Different Viruses Among Singapore Military Recruits 2009–2014

Cited by 13 publications

References 27 publications

Tissue-Resident Memory T Cells in the Lungs Protect against Acute Respiratory Syncytial Virus Infection

Tissue-Resident Memory T Cells in the Lungs Protect against Acute Respiratory Syncytial Virus Infection

Race and 1918 Influenza Pandemic in the United States: A Review of the Literature

TLR Agonists as Mediators of Trained Immunity: Mechanistic Insight and Immunotherapeutic Potential to Combat Infection

Contact Info

Product

Resources

About