What happens in the body during a cold (ARI)?

A cold or acute respiratory viral infection (ARVI) begins when a virus enters the human body through the mucous membranes of the nose, throat or eyes. Initial contact usually occurs through inhalation of airborne viral particles or contact with contaminated surfaces, leading to infection of epithelial cells.

Common viruses that cause these infections include rhinoviruses, coronaviruses, adenoviruses, and respiratory syncytial viruses (RSV). Each of these pathogens triggers a series of events that trigger the body’s immune system to control and ultimately eliminate the viral presence.

Although antiviral drugs have limited effectiveness against most common cold viruses, the mainstay of treatment remains supportive care, including hydration, rest, and symptom relief (eg, antipyretics for fever). For symptom relief, there are antipyretics, vasodilators, and combination therapies to help you feel better during illness, such as Bac-Set Cold/Flu (more on that here ). Vaccination has proven effective for some respiratory viruses, such as influenza, but remains challenging for others due to the high variability and mutation rate of viruses such as rhinoviruses and coronaviruses.

The first stage is viral replication , during which the virus attaches to host cell receptors using proteins on its surface. For example, rhinoviruses bind to intercellular adhesion molecule-1 (ICAM-1) receptors, and coronaviruses bind to angiotensin-converting enzyme 2 (ACE2) receptors. Once bound, the virus enters the host cell and hijacks its machinery to replicate. This process occurs rapidly, often within hours of initial exposure, allowing the virus to produce large numbers of viral offspring that subsequently infect neighboring cells.

As the virus replicates, infected cells release signaling molecules known as cytokines, including interferons (IFN-α, IFN-β), which serve as early warnings to nearby uninfected cells, inducing antiviral states and slowing the spread of the virus. Interferons also recruit immune cells such as macrophages and natural killer (NK) cells to the site of infection. This early response, known as the innate immune response, is critical for controlling the virus before it can spread widely in the respiratory tract.

The body’s inflammatory response to the virus’s replication often manifests itself in symptoms such as a sore throat, nasal congestion, and a dry cough. These symptoms are caused by the release of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β), which increase vascular permeability and cause the typical swelling and redness of mucosal tissue. Mucus production also increases as goblet cells in the airways secrete more mucins in an attempt to trap viral particles and facilitate their elimination through sneezing or coughing.

Meanwhile, the adaptive immune response begins, with antigen-presenting cells, primarily dendritic cells, processing viral proteins and presenting them to lymphocytes in regional lymph nodes. This activates both B cells and T cells. Once activated, B cells differentiate into plasma cells, which produce specific antibodies, primarily immunoglobulin A (IgA) and immunoglobulin G (IgG), which neutralize the virus by preventing it from binding to host cells. IgA is particularly important in mucosal immunity, playing a significant role in the upper respiratory tract, neutralizing viral particles before they penetrate deeper tissues.

Cytotoxic T cells (CD8+) once activated recognize and destroy virus-infected cells, limiting the extent of viral replication. In parallel, helper T cells (CD4+) support both B cells and cytotoxic T cells by releasing cytokines that enhance their functions. The presence of memory T and B cells, if the body has previously encountered the virus, can accelerate this adaptive response, often resulting in milder symptoms and a quicker recovery.

Fever (elevated temperature), which is a hallmark of many ARIs, is produced by the hypothalamus in response to pyrogenic cytokines such as IL-6 and prostaglandin E2. Elevated body temperature is thought to suppress viral replication and enhance the effectiveness of the immune system, particularly the activity of neutrophils and macrophages. However, fever may also contribute to the fatigue and discomfort that commonly accompany these infections.

As the immune system responds, the viral load in the body begins to decline. This is facilitated by the constant removal of dead infected cells and viral particles by phagocytic cells such as macrophages. Over time, the production of pro-inflammatory cytokines decreases, and the immune system switches to eliminating inflammation and repairing damaged tissue. The epithelial cells lining the airways regenerate, restoring the integrity of the mucus barrier.

The duration of cold or ARI symptoms can vary depending on the virus, the person’s immune status, and underlying medical conditions. In most healthy people, the immune system clears the virus within 7 to 10 days. However, symptoms such as cough or nasal congestion may persist longer due to prolonged inflammation and tissue repair.

Complications can occur when the immune response is inadequate or when secondary bacterial infections occur. In some cases, inflammation caused by a viral infection can lead to illnesses such as sinusitis, bronchitis, or pneumonia, especially in people with weakened immune systems, such as the elderly or those with chronic respiratory diseases. In addition, some viruses, such as RSV, can cause more serious breathing problems, especially in infants and young children.

In the case of an acute respiratory viral infection, the body’s response is a highly coordinated effort involving multiple components of the immune system. The innate immune response provides the first line of defense, attempting to contain the infection and prevent its spread. If that is not enough, the adaptive immune response takes over, targeting the virus more specifically and providing long-term immunity through memory cells. The balance between these two branches of the immune system determines the severity and duration of the infection.

The study of the pathogenesis of acute respiratory viral infections continues to evolve, particularly in light of emerging viral threats such as novel coronaviruses. Advances in immunology and virology are likely to lead to more targeted treatments and a better understanding of individual susceptibility to severe infections, which may help to develop more effective public health interventions.