Severe acute respiratory syndrome (SARS) is caused by infection with a specific type of coronavirus known as SARS-CoV. This virus belongs to the coronavirus family, which are single-stranded RNA viruses characterized by their crown-like spikes on the surface. The primary cause of SARS is the entry and replication of this virus in human respiratory cells, leading to severe lung inflammation and damage.
The process begins when the virus uses its distinctive spike proteins to attach itself to receptors on human cells. For SARS-CoV, these receptors are primarily angiotensin-converting enzyme 2 (ACE2) molecules found on the surface of various cell types, especially those lining the respiratory tract. Once attached, the viral membrane fuses with that of the host cell, allowing viral RNA to enter inside.
Inside the host cell, this viral RNA hijacks cellular machinery for its own replication. The host’s ribosomes read and translate viral RNA into long chains called polyproteins—these are like strings made up of smaller functional units called nonstructural proteins. These units then separate and assemble into complexes that replicate more copies of viral RNA and produce structural components needed for new virus particles.
As new viruses multiply within infected cells, they cause direct injury by disrupting normal cellular functions and triggering immune responses. The immune system detects infected cells and mounts an inflammatory reaction aimed at clearing infection but often causes collateral tissue damage in lungs. This inflammation leads to symptoms such as fever, cough, difficulty breathing, and can progress rapidly into pneumonia or acute respiratory distress syndrome (ARDS), which severely impairs oxygen exchange.
Beyond just lung tissue involvement, SARS-CoV can affect other organs where ACE2 receptors exist—such as gastrointestinal tract cells or even testicular Leydig cells—by similar mechanisms: binding via spike protein followed by intracellular replication causing local dysfunctions.
Several factors contribute further to disease severity:
– **Immune dysregulation:** Sometimes immune responses become excessive or misdirected causing a “cytokine storm,” an overwhelming release of inflammatory molecules damaging tissues beyond control.
– **Virus-host interactions:** Viral proteins interact with multiple human proteins involved in inflammation regulation or cellular survival pathways; some may help virus evade immunity or promote persistent infection.
– **Metabolic hijacking:** Infected cells’ metabolism is altered; for example in hormone-producing testicular cells cholesterol storage is exploited by viruses for building new particles.
– **Transmission dynamics:** Virus spreads mainly through droplets expelled during coughing or sneezing from infected individuals; these droplets carry infectious particles capable of infecting others upon inhalation.
In summary: Severe acute respiratory syndrome arises when SARS coronavirus attaches via spike protein to ACE2 receptors on human airway epithelial cells; it then enters these cells using membrane fusion mechanisms allowing its RNA genome inside where it commandeers ribosomes producing polyproteins that cleave into functional units essential for replicating new viruses; this leads to widespread cell injury combined with intense immune-mediated inflammation resulting in severe lung pathology characteristic of SARS disease manifestation across multiple organ systems expressing ACE2 receptor sites including lungs but also gastrointestinal tract and reproductive organs under certain conditions—all contributing collectively toward clinical severity seen during outbreaks caused by this pathogen.
