Coughing is commonly not from the common cold
A leading cause of respiratory disease in children is Respiratory Syncytial Virus (RSV), producing over 3 million cases of lower respiratory illness and about 100,000 deaths annually (Nair et al. 2010). RSV is classified as a virus in the family Paramyxoviridae, which are all non-segmented negative sense RNA viruses. Other viruses that utilize this method of replication include Mumps virus, Human Metapneumovirus (hMPV), and Henipavirus, the inspiration of the movie Contagion. Like most viruses that cause respiratory symptoms, including viruses that cause common cold, numbers of RSV infections increase in winter months when people spend more time indoors (Florida is weird).
Nearly all children will encounter RSV, but only 2-3% will require hospitalization. However, the real trouble is re-infection. Typically after your immune system develops antibodies against an antigen, it can recall the “memory” of the infection to produce specific antibodies and lymphocytes to prevent re-infection by the same agent. However, this “memory” can fade, and is of particular concern with RSV.
Challenge experiments have shown that 73% of adults became reinfected a second time within 26 months, and 43% became reinfected a third time with apparent symptoms in the majority of the cases (Hall et al. 1991). In short, the virus is capable of reinfecting healthy individuals, and immunity is relatively short-lived. This also makes it particularly difficult to produce a vaccine that does not need to be administered annually.
An appropriate adaptive immune response requires the activity of dendritic cells (DCs). In short, DCs are antigen presenter cells, and direct the T-cell and B-cell response at a particular target. DCs move from a site of infection to the lymph nodes in order to activate the proliferation of the proper lymphocytes to defend against a particular pathogen (a short video is provided below). DC migration is directed primarily by chemokines, or signalling proteins that the DC recognizes through the receptor CCR7. Without CCR7, the DC’s ability to detect chemokines is severely diminished, and without migration to the lymph node, downstream activation of the adaptive immune response is absent.
In the 2011 paper in PLOS Pathogens by Nouen et al., the authors demonstrate that RSV infection leads to a decrease in the expression of CCR7 in DCs during infection. RSV alters dendritic cell migration, and reduces DC migration to the lymph nodes.I This finding suggests that RSV is capable of regulating the immune response by reducing the activation of lymphocytes. Measles virus, another paramyxovirus, has also been shown inhibit DC migration through the modulation of CCR7 expression.
I would again like to highlight the incredible adaptability of pathogens to persist in an environment. Viruses have evolved to persist in even the harshest of all environments, including the human immune system, which is tasked with the very specific job of fighting these viruses.
Despite being known as a clinically significant human pathogen since the 1950s, a vaccine for RSV is still unavailable. However, a better understanding of how RSV modulates immunity gives us a clearer picture of why RSV vaccine development is so difficult. In contrast to Ebolavirus, RSV is very well adapted to humans, and rarely kills its host, but the disease burden of RSV is certainly significant.
Fortunately, basic research into mechanisms of pathogenesis is leading us in the right direction. But what you may believe to be a “common cold” (which may actually be caused by any number of viruses including rhinovirus, adenovirus, or coronavirus) can be RSV. Persistent infection should have you worried, but at least it’s not Ebola.