Abstract
Induction of autophagy has been shown to be beneficial for the replication of poliovirus, a phenomenon that might also apply for other picornaviruses. We demonstrate that de novo synthesis of human rhinovirus type 2 (HRV2), an HRV of the minor receptor group, is unaffected by tamoxifen, rapamycin, and 3-methyladenine (3-MA), drugs either stimulating (tamoxifen and rapamycin) or inhibiting (3-MA) autophagic processes. Furthermore, LC3-positive vesicles (i.e., autophagosomes) are not induced upon infection. Therefore, multiplication of this particular picornavirus is not dependent on autophagy.
Highlights
Induction of autophagy has been shown to be beneficial for the replication of poliovirus, a phenomenon that might apply for other picornaviruses
We demonstrate that de novo synthesis of human rhinovirus type 2 (HRV2), an Human rhinoviruses (HRVs) of the minor receptor group, is unaffected by tamoxifen, rapamycin, and 3-methyladenine (3-MA), drugs either stimulating or inhibiting (3-MA) autophagic processes
Upon infection (Fig. 2B), virus-producing cells were revealed with monoclonal anti-HRV2 antibody (8F5; 1:500) [2]
Summary
Induction of autophagy has been shown to be beneficial for the replication of poliovirus, a phenomenon that might apply for other picornaviruses. Induction of autophagy by tamoxifen and rapamycin increased poliovirus yield [6]. Based on immunofluorescence colocalization of green fluorescent protein (GFP)-microtubule-associated protein light chain kinase 3 (LC3) (an autophagosome marker) and LAMP-1 as well as staining with monodansylcadaverine (MDC), autophagosomes were observed after infection with HRV2 and the major-group virus HRV14.
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