Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Jul;57(4):809-16.
doi: 10.3349/ymj.2016.57.4.809.

In Hot Pursuit of the First Vaccine Against Respiratory Syncytial Virus

Joo Young Kim  1 , Jun Chang  2
Affiliations
Review

In Hot Pursuit of the First Vaccine Against Respiratory Syncytial Virus

Joo Young Kim et al. Yonsei Med J. 2016 Jul.

Abstract

Human respiratory syncytial virus (RSV) is the leading cause of severe lower respiratory tract infection, such as bronchiolitis, bronchitis, or pneumonia, in both infants and the elderly. Despite the global burden of diseases attributable to RSV infection, no clinically approved vaccine is available, and a humanized monoclonal antibody for prophylaxis is not readily affordable in developing countries. There are several hurdles to the successful development of RSV vaccines: immune-vulnerable target populations such as premature infants, pregnant women, and immunocompromised people; safety concerns associated with vaccine-enhanced diseases; repeated infection; and waning memory. To develop successful strategies for the prevention of RSV infection, it is necessary to understand the protective and pathologic roles of host immune responses to RSV infection. In this review, we will summarize the positive and negative relationship between RSV infection and host immunity and discuss strategies for the development of the first successful RSV vaccine.

Keywords: Immunity; respiratory syncytial viruses; vaccine; vaccine-enhanced diseases.

PubMed Disclaimer

Conflict of interest statement

The authors have no financial conflicts of interest.

Figures

Fig. 1
Fig. 1. RSV genome, proteins, and their functions. In the schematic diagram of the RSV genome, 10 genes are indicated in the order NS1-NS2-N-P-M-SH-G-F-M2-L. Filled square, genes encoding proteins targeted by neutralizing antibodies. (A) Simplified diagram of RSV F protein-mediated membrane fusion. (B) Attachment of RSV G protein to the host cell membrane is mediated by HS and HBD and/or the CX3C-CX3CR1 interaction. Pre-fusion, pre-fusion form of the F protein; Intermediate, refolding of the F protein to initiate membrane attachment; Post-fusion, membrane fusion between RSV and the target cell; HS, heparan sulfate; HBD, heparin-binding domain; RSV, respiratory syncytial virus.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Hall CB, Walsh EE, Long CE, Schnabel KC. Immunity to and frequency of reinfection with respiratory syncytial virus. J Infect Dis. 1991;163:693–698. - PubMed
    1. Volling C, Hassan K, Mazzulli T, Green K, Al-Den A, Hunter P, et al. Respiratory syncytial virus infection-associated hospitalization in adults: a retrospective cohort study. BMC Infect Dis. 2014;14:665. - PMC - PubMed
    1. Bhoj VG, Sun Q, Bhoj EJ, Somers C, Chen X, Torres JP, et al. MAVS and MyD88 are essential for innate immunity but not cytotoxic T lymphocyte response against respiratory syncytial virus. Proc Natl Acad Sci U S A. 2008;105:14046–14051. - PMC - PubMed
    1. Kawai T, Akira S. TLR signaling. Semin Immunol. 2007;19:24–32. - PubMed
    1. Rudd BD, Smit JJ, Flavell RA, Alexopoulou L, Schaller MA, Gruber A, et al. Deletion of TLR3 alters the pulmonary immune environment and mucus production during respiratory syncytial virus infection. J Immunol. 2006;176:1937–1942. - PubMed

MeSH terms

Substances