Therefore, CHLA and PUG are able to abrogate host cell binding and penetration by HCMV, HCV, DENV-2, MV, and RSV during the cell entry process. Control of virus spread post-infection by CHLA and PUG We next determined the

antiviral activity of the two hydrolyzable tannins in controlling spread of established infections. Target cell monolayers were infected with the respective test virus, and then incubated with or without the compounds. As shown in Figure 6, both CHLA and PUG effectively inhibited MI-503 price HCMV, HCV, and MV infections (80 – 100% protection), but were ineffective against the growth of DENV-2 and RSV (< 25%). To further validate the tannins’ effect on virus cell-to-cell transmission, we examined the effects of the drugs on viral plaque size. The change in the area of the plaques was measured using either viral immunofluorescence or EGFP-tagged reporter viruses. Neutralizing antibodies, methylcellulose or this website agarose were included in the overlay medium to prevent secondary infection of uninfected cells throughout the monolayer, ensuring that viral spread occurs

via intercellular junctions between neighboring infected and virus-free populations. The data indicated

that viral plaques from HCMV, HCV, and MV infections were restricted by CHLA and PUG to near initial size, whereas plaques due to DENV-2 and RSV infections were unaffected and expanded further (Figure 7 and Additional file 1: Figure S1, Additional file 2: Figure S2, Additional Cediranib (AZD2171) file 3: Figure S3, Additional file 4: Figure S4 and Additional file 5: Figure S5). These results are in agreement with the data obtained following post-entry drug treatment in Figure 6, where HCMV, HCV, and MV, but not DENV-2 and RSV, were shown to be sensitive to the tannins’ antiviral effects. Thus, it appears that the two tannins are effective in limiting post-infection spread of HCMV, HCV, and MV, but are inefficient in preventing cell-to-cell transmission of DENV-2 and RSV. Heparin, on the other hand, displayed limited effect against the spread of the viruses post-entry (Figures 6 and 7). The window of antiviral activity from CHLA, PUG, and heparin at different stages of viral entry and spread are summarized in Table 3.