The COVID-19 pandemic is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Understanding the “COVID particle” helps explain its effects and how it spreads.
Anatomy of the SARS-CoV-2 Particle
The SARS-CoV-2 virus particle, also known as a virion, is a spherical, enveloped entity approximately 60–140 nanometers in diameter. At its core, it contains a single-stranded RNA genome, its genetic blueprint. This RNA is tightly bound by nucleoproteins, forming a helical nucleocapsid structure that provides stability to the genetic material.
Surrounding the nucleocapsid is a viral envelope, a lipid bilayer derived from the host cell, a protective outer layer. Embedded within this envelope are three additional structural proteins: the membrane (M) protein, the envelope (E) protein, and the spike (S) glycoprotein. The M protein is the most abundant and is involved in virus assembly and shaping the viral envelope. The E protein also contributes to assembly and release, and is known to form ion channels.
The most recognizable features on the viral surface are the bulbous projections formed by the spike (S) glycoproteins, giving coronaviruses their crown-like appearance, hence the name “corona.” These spike proteins are necessary for the virus to infect human cells. Each spike protein is a homotrimer, composed of two subunits, S1 and S2, which play distinct roles in the infection process.
How the Particle Spreads
The SARS-CoV-2 particle primarily spreads from person to person through respiratory droplets and aerosols expelled by infected individuals during activities such as breathing, talking, coughing, or sneezing. Droplets are larger particles, greater than 5 micrometers in diameter, which tend to fall out of the air relatively quickly, within a short distance of the infected person. These can directly contact the mucous membranes of another individual, leading to infection.
Aerosols, conversely, are smaller particles, less than 5 micrometers, that can remain suspended in the air for longer periods and travel greater distances, particularly in indoor environments with poor ventilation. While direct contact with larger droplets is a common mode of transmission, airborne transmission via aerosols, especially in specific circumstances like aerosol-generating procedures or poorly ventilated spaces, is a recognized pathway.
Transmission can also occur through contact with contaminated surfaces, known as fomites, though this is considered a less frequent mode compared to airborne spread. Fomites become contaminated when respiratory droplets or secretions land on them, and a person then touches the contaminated surface and their eyes, nose, or mouth. Public health measures like hand hygiene and surface cleaning are aimed at reducing this type of transmission.
How the Particle Infects Cells
The infection process begins when the SARS-CoV-2 particle encounters a susceptible human cell. The spike (S) glycoprotein on the virus surface plays a role in this initial interaction. A region within the S1 subunit of the spike protein, called the receptor-binding domain (RBD), directly binds to the angiotensin-converting enzyme 2 (ACE2) receptor on human cells. ACE2 receptors are found on various cell types throughout the body, with higher concentration in lung cells, making the respiratory system a primary target.
Upon binding to the ACE2 receptor, the spike protein undergoes a change in its three-dimensional structure, a necessary step for the virus to gain entry into the cell. Host cell enzymes, such as TMPRSS2 and furin, cleave the spike protein at specific sites, enabling this structural rearrangement and promoting fusion of the viral membrane with the host cell membrane. This fusion allows the viral RNA genome to be released into the cytoplasm of the human cell, where the virus replicates and produces new viral particles. The virus hijacks the cell’s machinery to create more copies.
Particle Survival Outside the Body
The SARS-CoV-2 particle can remain infectious on various surfaces and in the air for different durations, influenced by environmental factors. In aerosolized form, the virus is viable for up to 3 hours in laboratory settings. On surfaces, its survival time varies depending on the material.
The virus remains detectable on plastic surfaces for up to 72 hours and on stainless steel for up to 48 hours, though its infectious titer may decrease over time. On porous surfaces like cardboard, the virus’s viability is shorter, detectable for up to 24 hours. Copper surfaces inactivate the virus more quickly, with viability lasting around 4 hours.
Temperature and humidity play a role in the virus’s persistence outside the body. Higher temperatures, around 93 degrees Fahrenheit, can degrade the outer structure of the virus, making it less infectious. Conversely, cooler temperatures, like room temperature or outdoor winter conditions, can allow the virus to remain infectious for longer periods on surfaces. Humidity, while impacting how far respiratory aerosols travel, has shown less influence on the virus’s survival directly on surfaces.
Impact of Viral Variants on the Particle
The SARS-CoV-2 particle is subject to continuous mutation, leading to new viral “variants.” These mutations can alter the characteristics of the virus particle, influencing its behavior and interaction with human hosts. Mutations in the spike protein are notable because this protein is responsible for binding to human cells and is a main target for immune responses and vaccines.
Changes in the spike protein can lead to increased transmissibility, making the variant spread more easily. Some mutations can enhance the spike protein’s binding affinity to the ACE2 receptor on human cells, making the virus more efficient at initiating infection. Other mutations enable the virus to evade the immune system’s defenses, including antibodies developed from previous infections or vaccinations.
These alterations can affect how existing antibodies recognize and neutralize the virus. While many mutations are neutral, those that confer a selective advantage, like improved binding or immune evasion, are more likely to become prevalent. The continuous evolution of the virus highlights the need for ongoing monitoring and adaptation of public health strategies.