Caffeine:
Preliminary reports showed caffeine as a potential antiviral agent with
its antiviral effect on certain viruses like the influenza virus,
poliovirus, herpes simplex virus type 1 (HSV-1), and vaccinia virus
(Yamazaki and Tagaya 1980). Subsequent
studies showed that caffeine also inhibited viral RNA synthesis and
viral protein synthesis in infected cells and thereby inhibiting growth
and propagation of Newcastle disease virus (NDV), HSV-1, human
immunodeficiency virus, vaccinia virus and polyomavirus
(Olson and Consigli 1979;
Shiraki and Rapp 1988;
Dahl et al. 2005;
Daniel et al. 2005). Caffeine was
reported to inhibit the protein synthesis of HSV-1, which suppressed the
formation of HSV-1 plaques by interfering with the cell-cell
transmission of HSV-1 (Shiraki and Rapp
1988). Later it was further confirmed by the quantitative
characterization that caffeine preferentially causes cytopathic effect
(CPE) and the death of HSV-1 infected cells
(Murayama et al. 2008). Therefore, such
preferential CPE of caffeine on virally infected cells raises the
potential of SARS-CoV-2 infected patient cells as caffeine could
potentially reduce the viral load and also could induce selective death
of virus-infected cells of COVID-19 patients. However, it is very
important to note that caffeine-induced increased CPE and cell death was
not detected for influenza virus and poliovirus and this was probably
because these two viruses generally induced rapid cell death of infected
cells immediately after infection and therefore masked the acceleration
of caffeine-induced CPE of virus-infected cells if any
(Murayama et al. 2008).
The aforementioned observation suggests that caffeine-induced selective
degeneration of virally infected cells may be dependent on the species
of the virus. In a more recent meta-analysis on the effect of caffeine
in patients with chronic hepatitis C, it was shown that patients with
higher caffeine intake showed 61% reduced risk of developing advanced
hepatic fibrosis and was also associated with lower serum ALT levels in
chronic hepatitis C patients compared to lower caffeine intake patient
group (Jaruvongvanich et al. 2017).
Specifically for hepatitis C, an in-vitro study also demonstrated that
caffeine efficiently inhibited the replication of hepatitis C
replication in a dose-dependent manner, further confirming the antiviral
potential of caffeine (Batista et al.
2015). Overall, there is compelling evidence for the broad-spectrum
antiviral role of caffeine, and its antiviral actions are well
characterized in several viral species, and it could play a critical
role in being a potential antiviral therapy in COVID-19 patients as well