The COVID19 virus has plagued the world, as a cellular and molecular biologist, I am presenting this commentary after careful analysis of the genomic structure of the virus and its effects on the lungs.Why does it affect the older generation more compared to young adults and children?The free radical theory of aging proposes that organisms age because they accumulate oxidative damage1-3. I postulate this causes the older population to have an increase in reactive oxygen species (ROS) 4-7, which partially reduces metabolites of molecular oxygen generated as by-products of various cellular processes, such as respiration1,8. This creates a condition of hypoxia, particularly in the lungs as the lung volume and capacity decreases with age9.Another interesting phenomena to note is that severe acute respiratory syndrome (SARS-CoV) virus, which is genetically similar to corona virus, are known to proliferate in hypoxia conditions. Hence, making the older generation more susceptible to disease.Another point to be noted is the lungs are highly vulnerable to viral infection as the express increased cell surface proteins that the viruses use to gain entry into the cell10. Latest research shows that ACE2 (Angiotensin-converting enzyme 2) has been identified as a potential SARS-CoV2 receptor and is highly expressed in the lungs11-12. One of the severe manifestations of corona virus is lung fibrosis, even when the patient is recovered, the lung function declines by 20-30%13-15. The initiation of lung fibrosis occurs as ROS species are generated by NADPH oxidase-4 (NOX4), the pathway it triggers is angiotensin II (AngII) type 1 receptor (AT1R) axis which causes increased ROS production in lung fibroblasts16. Angiotensin-converting enzyme 2 (ACE2) counteracts this inhibition via the RhoA/Rock pathway by reducing NOX4-derived ROS16. My hypothesis is that as the SARS-CoV2 virus enters the bloodstream, infecting the lung cells, it uses all the available ACE2 receptors, which causes an elevation in AngII-AT1R axis, which leads to activation of NOX4-derived ROS-mediated RhoA/Rock pathway, creating a hypoxic environment, this further facilitates viral multiplication and causes chronic obstructive in the lungs. Therefore, pharmacological antioxidants can act as potential drug targets in this scenario.In layman’s terms- for this virus to multiply, it requires hypoxic conditions and it creates this by attacking the lung surface protein that prevents hypoxia. Potentially, if we have more antioxidants in our body the lesser chance of the virus finding the ideal conditions to proliferate.