COVID-19 has led on to a global healthcare crisis, similar to none in the recent past. Special emphasis must be laid on the impact of the infection on patients with COPD and Asthma, considering the vulnerability seen in these groups toward previous coronavirus diseases. SARS-CoV-2 is known to be utilizing angiotensin-converting enzyme 2 (ACE2) receptors to infect humans hosts. Moreover, the pathological findings of COVID-19, is diffuse alveolar damage with fibrin rich hyaline membranes and a few multi-nucleated giant cells. Both of which indicate towards the detrimental impacts the infection on outcomes in COPD and Asthma patients. There have been previous studies on how patients with asthma and COPD have differing outcomes based on the different ACE2 expressions, specifically in the lower airways, and over here, through this presentation, we will understand the possible differing outcomes and the immunological basis behind them. Within this presentation, we will try to understand the the mechanisms that seed infection distally in the lungs, and the virus-host interactions that attenuate or augment intra-regional virus growth in the lungs of COPD patients to produce severe disease.