Development and Progression of the Common Cold
While the common cold may be caused by over 200 distinct and continually evolving viral pathogens; rhinoviruses, coronaviruses and respiratory syncytial viruses appear to be some of the most common (Turner 2009; Nussenbaum 2010; Worrall 2011; CDC 2012C).
Infection occurs when the cold-causing virus comes into contact with mucous membranes in the nose or eyes. Common cold infections generally result in a non-specific acute inflammatory response that stimulates the release of various inflammatory cytokines and other immune mediators. In fact, many of the symptoms associated with the common cold are a result of inflammation caused by this immune response, rather than by the virus itself (Turner 2009; Turner 2011; Hayden 2011; Pappas 2009). For example, the release of a proinflammatory peptide called bradykinin is a major contributor to sore throat symptoms (Turner 2009; Proud 1988). Stuffy nose symptoms result from increased pooling of blood in nasal blood vessels and increased nasal secretions. Likewise, runny nose occurs due to enhanced permeability of nasal blood vessels, which allows serum to leak into the nasal mucosa (Turner 2011).
Although infection with a virus known to cause the common cold generates an adaptive immune response that helps protect against repeated infection by the same or very similar virus, the sheer volume of distinct viruses that can cause the common cold makes developing immunity against the common cold itself very challenging (Hayden 2011; Turner 2009, Turner 2011). However, infection by a cold virus can decrease the risk and severity of re-infection with the same virus (Turner 2009).
New Understanding of the Human Immune System Paves Way for Potential Common Cold Treatment
For at least the last 100 years it has been assumed that the ability of antibodies produced by the immune system to protect against pathogens ends at the cellular membrane. In other words, scientists have thought that once a virus enters a cell it escapes the attack of antibody-mediated immunity, leaving only one option to eliminate the virus – kill the cell that harbors it. However, emergent research suggests this is not the case.
A specialized protein within cells called TRIM21 has been shown to bind to virus-bound antibodies within the cell and initiate an intracellular immune response (McEwan 2011).
Researchers have proposed that delivery of exogenous TRIM21, perhaps as a nasal spray, may help up-regulate immunity against some cold-causing viral pathogens and eliminate them in as little as a few hours (Mallery 2010; Connor 2010).
Although more research is needed before these findings can be applied clinically, the discovery of an intracellular defense system against viruses opens the door to promising new interventions for the common cold and other viral diseases.