The penetration of various viruses into host cells is accomplished by hijacking the host endocytosis machinery. In the case of severe acute respiratory syndrome coronavirus (SARS-CoV) infection, viral entry is reported to require a low pH in intracytoplasmic vesicles; however, little is known about how SARS-CoV invades such compartments. Here we demonstrate that SARS-CoV mainly utilizes the clathrin-mediated endocytosis pathway for its entry to target cells by using infectious SARS-CoV, as well as a SARS-CoV pseudovirus packaged in the SARS-CoV envelope. The SARS-CoV entered caveolin-1-negative HepG2 cells, and the entry was significantly inhibited by treatment with chlorpromazine, an inhibitor for clathrin-dependent endocytosis, and by small interfering RNAmediated gene silencing for the clathrin heavy chain. Furthermore, the SARS-CoV entered COS7 cells transfected with the mutant of ACE2 with the cytoplasmic tail deleted, SARS-CoV receptor, as well as the wild-type ACE2, and their entries were significantly inhibited by treatment with chlorpromazine. In addition, ACE2 translocated into EEA1-positive early endosomes immediately after the virus attachment to ACE2. These results suggest that when SARS-CoV binds ACE2 it is internalized and penetrates early endosomes in a clathrin-dependent manner and that the cytoplasmic tail of ACE2 is not required for the penetration of SARS-CoV.

We found that the butanol fraction of Cinnamomi Cortex (CC/Fr.2) showed moderate inhibitory activity in wild-type severe acute respiratory syndrome coronavirus (wtSARS-CoV) and HIV/SARS-CoV S pseudovirus infections. The inhibition on pseudovirus was also seen in cells pretreated with the CC and CC/Fr.2 (IC(50S), 283.4+/-16.3 and 149.5+/-13.5 microg/ml, respectively), however the highest activities on wtSARS-CoV were observed when the viruses were treated by the extracts before challenging (IC(50S), 43.1+/-2.8 and 7.8+/-0.3 microg/ml; SIs, 8.4 and 23.1, respectively). Among the compounds fractionated from CC, procyanidin A2 and procyanidin B1 showed moderate anti-wtSARS-CoV activity (IC(50S), 29.9+/-3.3 and 41.3+/-3.4 microM; SIs, 37.35 and 15.69, respectively). We also sought to determine whether they could interfere with the clathrin-dependent endocytosis pathway using transferrin receptor (TfR) as an indicator. CC/Fr.2 inhibited the internalization of TfR but the procyanidins did not. Taken together, CC/Fr.2 contains unknown substances, that could inhibit the infection, probably by interfering with endocytosis, and it also contains procyanidins that did not inhibit the internalization but inhibited the infection. Therefore, CC extracts contain anti-virus activities that act through distinct mechanisms according to differences in the compounds or mixtures.

While protective measures in response to infectious diseases may reduce the freedom of tourists (regarding their behaviors), few studies have documented the effects of destination protective measures on the self-protective behaviors of tourists. By applying the protection motivation theory, this study examines the effects of perceived destination protective supports on the social distancing intentions of tourists during the COVID-19 pandemic. The results reveal significant relationships among perceived destination support, coping appraisal, threat appraisal, and the social distancing intentions of tourists. Moreover, two cognitive appraisals—toward the pandemic—partially mediate the relationship between perceived destination support and social distancing intention, and this mediational process is ‘intervened’ with by social norms. This has implications on whether tourist destinations apply more rigorous social distancing polices during the COVID-19 pandemic, to enhance the coping confidence behaviors of tourists, without causing anxiety and fear, and to achieve the goal of enhancing tourists’ intentions to protect themselves.

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