Decreased smell function is related to brain health, future mortality, and quality of life. Most people inflicted with the SARS-CoV-2 virus evidence some measurable smell dysfunction during its acute phase, although many are unaware of the loss. Long-term deficits occur in up to 30% of COVID-19 cases, although total anosmia is relatively rare. This review explores what is presently known about the nature and pathophysiology of olfactory dysfunction due to the SARS-CoV-2 virus, including reversible inflammation within the olfactory cleft, downregulation of olfactory receptor proteins, and long-lasting peripheral and central damage to olfactory structures. It also addresses the question as to whether long-term smell loss might increase the likelihood of future development of cognitive and neurological deficits. COVID-19 has brought to public attention the importance of the sense of smell in everyday life, with untold numbers of patients seeking treatment for decreased ability to smell, which, in many cases, may be permanent.The neuroepithelium that harbors the olfactory receptor cells is directly exposed to the outside environment, making it susceptible to damage from toxic agents and a host of viruses, most notably SARS-CoV-2, the cause of COVID-19.SARS-CoV-2 invades nearly all types of cells within the olfactory neuroepithelium, but does not appear to significantly invade olfactory receptor cells, which lack the primary entry receptor, angiotensin-converting enzyme II (ACE2). However, other entry receptors may also be involved.The degree to which SARS-CoV-2 impacts central olfactory processing centers or leads to later neurological disorders has yet to be determined.