Age-Related Development of Human Memory T-Helper and B-Cell Responses toward Parainfluenza Virus Type-1

Smith, Falconer; Portner, Allen; Leggiadro, Robert J.; Turner, Emma; Hurwitz, Julia L.

doi:10.1006/viro.1994.1665

Cited by 33 publications

(22 citation statements)

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“…This cross-reactivity applies to virus-specific B-and T-cells, and targets several distinct viral proteins. 13,14 SeV is pathogenic in mice, but is not known to cause disease in humans; SeV is now being developed as a xenotropic vaccine administered intranasally to prevent hPIV-1 infection or disease, and also as a delivery system (vector) for antigens from other human viruses including hPIV-3, 15 hPIV-2, 16 and RSV [17][18][19][20] and more recently for HIV. [21][22][23][24] SeV is also used as a vector to deliver human fibroblast growth factor 2, 25 and angiopoietin-1, 26 genes for the treatment of peripheral artery disease, oncolytic virotherapy, 27 and cancer immunotherapy.…”

Section: Discussionmentioning

confidence: 99%

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Prevalence of specific neutralizing antibodies against Sendai virus in populations from different geographic areas: Implications for AIDS vaccine development using Sendai virus vectors

et al. 2011

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Section: Discussionmentioning

confidence: 99%

“…This result indicates that antibodies induced by natural infection with hPIV-1 do cross-react with SeV and neutralize its infectivity. 12,13 SeV NAb were detected in a majority of subjects ( Fig. 3) with an overall prevalence of 92.5% and a median titer of 60.6 (range: 5.9-11,324.7).…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 97%

Prevalence of specific neutralizing antibodies against Sendai virus in populations from different geographic areas: Implications for AIDS vaccine development using Sendai virus vectors

et al. 2011

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“…This assumption was reinforced by the observation of impaired IFN␥ T-cell responses associated with increased infectious risk to intracellular pathogens in early age (2)(3)(4)(5)(6)(7).…”

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confidence: 99%

Development of Cytomegalovirus and Adenovirus-Specific Memory CD4 T-Cell Functions From Birth to Adulthood

et al. 2011

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Age-related changes in memory CD4ϩ T cells (CD4) are poorly known. To address this issue, CD4 proliferative and cytokine responses to an anti-CD3 monoclonal (CD3), to cytomegalovirus (CMV), and to adenovirus (AdV) were assessed in 57 children (age, 0.07-17.16 y) and 17 adults. Results showed i) accumulation of memory CD4 with aging, with 2-3 times more centralmemory T cell (TCM; CD45RA Ϫ /CD62L ϩ ) than effector-memory T cell (TEM; CD45RA Ϫ /62L Ϫ ) CD4 at any age. ii) In children older than 2 y, CMV-specific CD4-secreting IFN␥ alone predominated over CD4-secreting IL2 ϩ IFN␥ and a continuous increase, with aging, in IFN␥ responses to the virus was observed. In contrast, in AdV infection, CD4-secreting IL2 ϩ IFN␥ predominated and IFN␥ responses to the virus reached adult levels from 3 y of age. iii) In children aged 0 -2 y, lower total IFN␥ responses to CMV (p Ͻ 0.02), AdV (p ϭ 0.05), and CD3 (p Ͻ 0.01) and lower IFN␥ ϩ IL2-responses (p ϭ 0.1, p Ͻ 0.02, p Ͻ 0.05, respectively) contrasted with no decrease in CD4-secreting IFN␥ alone. Defective proliferative responses to AdV (p ϭ 0.03) were also observed. In conclusion, the development of memory CD4 differed in acute AdV and persistent CMV infections. Young age seemed to depress mostly polyfunctional (IL2 ϩ IFN␥ secreting) CD4 in both infections. (Pediatr Res 69: 106-111, 2011)

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“…Sendai virus is the murine counterpart of human parainfluenza virus 1 (HPIV1), and these two viruses share high sequence homology and antigenic cross-reactivity (23,38,58). Both Sendai virus and HPIV1 cause respiratory diseases in their hosts that range from mild to severe, with the greatest morbidity and mortality occurring in immunocompromised hosts (3,17).…”

mentioning

confidence: 99%

Residues in the Heptad Repeat A Region of the Fusion Protein Modulate the Virulence of Sendai Virus in Mice

Luque¹,

Bridges²,

Mason³

et al. 2010

J Virol

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While the molecular basis of fusion (F) protein refolding during membrane fusion has been studied extensively in vitro, little is known about the biological significance of membrane fusion activity in parainfluenza virus replication and pathogenesis in vivo. Two recombinant Sendai viruses, F-L179V and F-K180Q, were generated that contain F protein mutations in the heptad repeat A region of the ectodomain, a region of the protein known to regulate F protein activation. In vitro, the F-L179V virus caused increased syncytium formation (cell-cell membrane fusion) yet had a rate of replication and levels of F protein expression and cleavage similar to wild-type virus. The F-K180Q virus had a reduced replication rate along with reduced levels of F protein expression, cleavage, and fusogenicity. In DBA/2 mice, the hyperfusogenic F-L179V virus induced greater morbidity and mortality than wild-type virus, while the attenuated F-K180Q virus was much less pathogenic. During the first week of infection, virus replication and inflammation in the lungs were similar for wild-type and F-L179V viruses. After approximately 1 week of infection, the clearance of F-L179V virus was delayed, and more extensive interstitial inflammation and necrosis were observed in the lungs, affecting entire lobes of the lungs and having significantly greater numbers of syncytial cell masses in alveolar spaces on day 10. On the other hand, the slower-growing F-K180Q virus caused much less extensive inflammation than wild-type virus, presumably due to its reduced replication rate, and did not cause observable syncytium formation in the lungs. Overall, the results show that residues in the heptad repeat A region of the F protein modulate the virulence of Sendai virus in mice by influencing both the spread and clearance of the virus and the extent and severity of inflammation. An understanding of how the F protein contributes to infection and inflammation in vivo may assist in the development of antiviral therapies against respiratory paramyxoviruses.

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Age-Related Development of Human Memory T-Helper and B-Cell Responses toward Parainfluenza Virus Type-1

Cited by 33 publications

References 0 publications

Prevalence of specific neutralizing antibodies against Sendai virus in populations from different geographic areas: Implications for AIDS vaccine development using Sendai virus vectors

Prevalence of specific neutralizing antibodies against Sendai virus in populations from different geographic areas: Implications for AIDS vaccine development using Sendai virus vectors

Development of Cytomegalovirus and Adenovirus-Specific Memory CD4 T-Cell Functions From Birth to Adulthood

Residues in the Heptad Repeat A Region of the Fusion Protein Modulate the Virulence of Sendai Virus in Mice

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