Rhinoviruses: Kinetics of ultraviolet inactivation and effects of UV and heat on immunogenicity

Hughes, John H.; Mitchell, Monica L; Hamparian, Vincent V.

doi:10.1007/bf01315018

Cited by 16 publications

(7 citation statements)

References 27 publications

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“…However, the same immunization schedule with nonirradiated, intact virus resulted in an antibody recognition pattern similar to that of UV-inactivated virus (data not shown). This is consistent with the similar antibody responses to intact and to UV-inactivated rhinovirus and poliovirus, which are, however, different from the antibody response induced by heat-inactivated virus (20). Therefore, the predominance of antibody response appears to be influenced in our studies primarily by the route of immunization rather than by potential structural differences resulting from UV inactivation.…”

Section: Discussionsupporting

confidence: 87%

Analysis of antibody responses to predominant linear epitopes of Theiler's murine encephalomyelitis virus

Inoue

Choe

Kim

1994

J Virol

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Using synthetic peptides, we have defined the major linear antibody epitopes of Theiler's murine encephalomyelitis virus (TMEV), i.e., AlA (VP11225), AlBa (VP1146.-160), AlCb (VP1262-276), A2A (VP22-16), A2B (VP2165,179), and A3A (VP324-37). A time course study with either pooled or individual sera indicates that susceptible SJL mice intracerebrally infected with TMEV strongly and selectively recognize the AlCb epitope of VP1, compared with resistant BALB/c or C57BL/6 mice, which broadly recognize most of the epitopes on the different capsid proteins. However, antibodies from SJL mice subcutaneously immunized with TMEV recognize primarily AlBa, AlCb, and A2A epitopes. A similar predominant recognition of the AlCb epitope was found with antibodies from the cerebrospinal fluid of intracerebrally virus-infected SJL mice. Interestingly, a substantial level of antibodies against the AlCb epitope in virus-infected SJL mice is of the immunoglobulin G2a subclass, in contrast to an undetectable level of this immunoglobulin G subclass in virus-immunized SJL mice. The level of in vitro viral neutralization by antibodies did not correlate with the clinical signs. Antibodies to AlCb, A2A, and A2B were able to neutralize viral plaque formation in vitro, while antibodies to A3A, AlA, and AlBa were not.

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Section: Discussionsupporting

confidence: 87%

Analysis of antibody responses to predominant linear epitopes of Theiler's murine encephalomyelitis virus

Inoue

Choe

Kim

1994

J Virol

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“…Pretreatment with UV irradiation not only affected RV replication but also completely abolished cytokine production, including IL-1␤, in the present study. UV irradiation blocks RV replication but not the capability to enter the cells (11). In a previous report by Terajima et al (31), monoclonal antibodies to ICAM-1 completely blocked RV14 infection when human tracheal epithelial cells were exposed to RV14 for 15 min.…”

Section: Discussionmentioning

confidence: 84%

“…To confirm that increases in cytokine production by RV14 infection were due to the effects of RV14 infection and not a contaminant present in the viral stock, the ability of UVinactivated virus to induce cytokine production was also examined. UV inactivation was performed as previously described (11).…”

Section: Downloaded Frommentioning

confidence: 99%

Effects of dexamethasone on rhinovirus infection in cultured human tracheal epithelial cells

Suzuki

Yamaya

Sekizawa

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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To examine the effects of glucocorticoid on rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with either RV2 or RV14. Viral infection was confirmed by demonstrating that viral RNA in infected cells and viral titers of supernatants and lysates from infected cells increased with time. RV14 infection upregulated the expression of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, on epithelial cells, and it increased the production of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor-alpha in supernatants. Dexamethasone reduced the viral titers of supernatants and cell lysates, viral RNA of infected cells, and susceptibility of RV14 infection in association with inhibition of cytokine production and ICAM-1 induction. In contrast to RV14 infection, dexamethasone did not alter RV2 infection, a minor group of RVs. These results suggest that dexamethasone may inhibit RV14 infection by reducing the surface expression of ICAM-1 in cultured human tracheal epithelial cells. Glucocorticoid may modulate airway inflammation via reducing the production of proinflammatory cytokines and ICAM-1 induced by rhinovirus infection.

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“…Second, the ability of ultraviolet (UV)-inactivated virus to induce cytokine production was also examined. UV inactivation was performed as described previously (26).…”

Section: Methodsmentioning

confidence: 99%

Infection of a human respiratory epithelial cell line with rhinovirus. Induction of cytokine release and modulation of susceptibility to infection by cytokine exposure.

Subauste¹,

Jacoby²,

Richards³

1995

J. Clin. Invest.

363

273

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Rhinovirus infections cause over one third of all colds and are a contributing factor to exacerbations of asthma. To gain insights into the early biochemical events that occur in infected epithelial cells, we develop, for the first time, a model in which a pure respiratory epithelial cell population can be routinely infected by rhinovirus. Viral infection was confirmed by demonstrating that viral titers of supernatants and lysates from infected cell increased with time and by PCR. Infection by rhinovirus 14 was inhibited by homotypic antiserum and by antibodies to intercellular adhesion molecule-i (ICAM-1), the receptor for this virus. Susceptibility of epithelial cells to infection by rhinovirus 14 (but not rhinovirus 2, an ICAM-1 independent strain) can be increased by preexposure of cells to TNFa, whereas IFNy reduces susceptibility to infection by both rhinovirus strains. Rhinovirus infection per se does not markedly alter ICAM-1 expression on epithelial cells. Finally, we demonstrate that rhinovirus infection induced increased production of IL-8, IL-6, and GM-CSF from epithelial cells. Production of IL-8 correlated with viral replication during the first 24 h after infection. This model should provide useful insights into the pathogenesis of rhinovirus infections. (J. Clin. Invest. 1995. 96:549-557.)

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Rhinoviruses: Kinetics of ultraviolet inactivation and effects of UV and heat on immunogenicity

Cited by 16 publications

References 27 publications

Analysis of antibody responses to predominant linear epitopes of Theiler's murine encephalomyelitis virus

Analysis of antibody responses to predominant linear epitopes of Theiler's murine encephalomyelitis virus

Effects of dexamethasone on rhinovirus infection in cultured human tracheal epithelial cells

Infection of a human respiratory epithelial cell line with rhinovirus. Induction of cytokine release and modulation of susceptibility to infection by cytokine exposure.

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