| Summary: | Rhinoviruses (RVs) are the leading cause of upper-respiratory tract infections in
humans. To date relatively little is known about the mechanism of RV infection and
no cure or prevention exists. Mounting evidence shows that RV replicates very little
in its host airway epithelial cells leading researchers to hypothesize that the illness
associated with RV infection is the result of the host's immune response, but not
necessarily RV replication. This study characterized RV infection in vitro in terms of
viral replication, viral RNA, and pro-inflammatory cytokine/chemokine secretion
over the course of a typical infection using two distinct airway epithelial cell lines
(BEAS-2B and A549) and two different receptor-utilizing RV serotypes (RV14 and
RV1A). Cells were infected with known amounts of RV, sampled over 1 week, and
assayed for infectious virus, RV14 RNA, and interleukin (IL)-6 and/or IL-8 secretion.
For BEAS-2B and A 549 cells viral replication peaked between day 1 (Dl) and D2
post-infection for both RV14 and RV1A, and no significant viral replication was
observed after D3. Stimulation of LL-6 and IL-8 was typically not observed before D2
and remained elevated up to D7. Overall, BEAS-2B cells were more susceptible to
RV infection than A549, and similar trends were observed for RV14 and RV1A,
except RV14 failed to replicate in the A549 cells. Furthermore, UV inactivation of
both RV serotypes completely inhibited viral replication and IL-6 secretion in the
BEAS-2B model, suggesting the necessity of genetically intact virus to stimulate the
IL-6 response. Finally, the effects of two chemically distinct Echinacea extracts on
viral replication and IL-6 secretion were investigated in the BEAS-2B model. Neither
of the Echinacea extracts had any effect on RV replication, nor did they stimulate IL-
6 secretion in uninfected cells. However, Echinacea treatment of RV infected cells
significantly affected IL-6 secretion, but a different trend was observed between RV
serotypes, and for the two herb preparations. Overall, RV infection of airway
epithelial cells results in relatively low levels of RV replication but a pronounced proinflammatory
cytokine/chemokine response which is the likely cause of cold
symptoms and a potential target for therapeutics. === Science, Faculty of === Zoology, Department of === Graduate
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