COVID-19 is caused by infection with SARS-CoV-2, a coronavirus belonging to the betacoronavirus genus. The virus contains a single-stranded RNA genome enclosed within a lipid envelope containing structural proteins, including the spike protein that gives coronaviruses their characteristic appearance. SARS-CoV-2 enters susceptible human cells through interactions involving its spike protein and cellular receptors, particularly ACE2. Once inside a cell, the virus redirects cellular processes to replicate its genome and produce viral proteins. New viral particles then spread to additional cells and can be expelled in respiratory secretions, allowing transmission between people. Thus, the immediate biological cause of COVID-19 is SARS-CoV-2 infection, while the severity of the resulting disease depends on viral, immune and host factors.
SARS-CoV-2 is transmitted principally through infectious respiratory particles. Infected people release particles when breathing, talking, singing, coughing or sneezing. Other people can become infected when they inhale infectious particles or when particles reach susceptible mucosal surfaces. Risk is greater at close range and in shared indoor environments, particularly when ventilation is poor. The amount of virus released varies between individuals and changes over the course of infection. People can transmit the virus before developing symptoms, and some people never develop noticeable symptoms, making transmission possible even when someone appears healthy. This characteristic contributed substantially to the difficulty of controlling SARS-CoV-2 transmission during the pandemic.
After inhalation, SARS-CoV-2 encounters cells lining the respiratory tract. Successful infection requires the virus to attach to and enter susceptible cells, replicate, assemble new virions and evade or withstand antiviral immune responses. The initial innate immune response includes interferons and other inflammatory pathways designed to restrict viral replication. Adaptive immunity subsequently generates antibodies and T-cell responses that can recognise viral components. Vaccination and previous infection can prime these responses, so subsequent infection may be controlled more rapidly and with less severe disease. This does not mean reinfection is impossible: immunity changes the risk and severity of disease rather than creating an absolute barrier against every future infection.
Viral evolution is an important component of COVID-19 epidemiology. SARS-CoV-2 accumulates genetic changes as it replicates and spreads. Most mutations have little effect, but some can alter properties such as transmissibility, immune escape, disease characteristics or the performance of diagnostic tests and treatments. WHO therefore monitors variants because the characteristics of the circulating virus can affect population-level risk and the effectiveness of public-health measures. Variant evolution does not change the fundamental answer to what causes COVID-19: the disease remains caused by SARS-CoV-2, although individual viral lineages can differ biologically.
Host factors strongly influence whether infection remains asymptomatic, produces mild disease or progresses to severe illness. Older age, certain chronic diseases, obesity, diabetes, cardiovascular or respiratory disease and weakened immunity are associated with higher risk of severe COVID-19. Previous vaccination and infection can reduce the probability of severe outcomes by providing immune memory. The relationship is probabilistic rather than absolute: healthy young people can occasionally become seriously ill, while high-risk individuals may experience only mild disease. Consequently, the presence of a risk factor does not cause COVID-19; infection with SARS-CoV-2 is necessary, while host characteristics modify the outcome after infection.
COVID-19 can involve both direct viral effects and immune-mediated tissue damage. In mild disease, viral replication may remain largely confined to the upper respiratory tract. In more severe cases, infection can involve the lower respiratory tract and produce pneumonia and impaired oxygen exchange. Excessive or dysregulated inflammation can contribute to tissue injury, vascular dysfunction and clotting abnormalities. Severe disease can therefore result from a combination of viral replication and the body's response to infection. This distinction explains why treatments for COVID-19 can include antiviral medicines that reduce viral replication and anti-inflammatory therapies that reduce damaging immune responses in appropriately selected hospitalised patients.
COVID-19 is not caused by influenza, ordinary bacteria, cold weather or antibiotics. Influenza and other respiratory viruses can produce similar symptoms, but they are caused by different pathogens. Bacterial infections can occur as complications or simultaneously with viral disease, but antibiotics do not kill SARS-CoV-2. Similarly, cold temperatures do not generate the virus, although environmental and behavioural factors can influence transmission by changing indoor crowding and ventilation. COVID-19 is acquired when a susceptible person becomes infected with SARS-CoV-2, primarily through exposure to infectious respiratory particles.
Prevention targets the transmission pathway and the probability of severe disease. Vaccination primes immune memory and remains an important tool for reducing severe COVID-19 outcomes. Improving ventilation reduces the concentration of infectious respiratory particles indoors, while avoiding close contact with infected people and using appropriate respiratory precautions can reduce exposure. Early diagnosis can matter for people at high risk because specific antiviral treatments may be available and generally work best when started early. WHO states that vaccination continues to provide strong protection against severe disease and death. COVID-19 therefore arises from a defined viral cause, but its population impact reflects a dynamic interaction between viral evolution, immunity, behaviour, environment, vaccination and individual risk factors.
