Why do we need a cure for the common cold?

April 6, 2016 3:04 pm

Why do we need a cure for the common cold?

by Dr Rob Lambkin-Williams, hVIVO

Well, from a personal perspective I am an asthmatic and although for you healthy souls a cold is just a minor inconvenience with a bit of a sniffle and sore throat, maybe a cough as well, for me it will makes my asthma much, much worse and I will usually end up on oral steroids at least twice a year.

The rest of the time, I am a healthy chap, I run half marathons, albeit slowly, but a full marathon is probably a few steps too far. Several groups have investigated why a tiny little virus should cause such issues for a certain proportion of the population, such as myself.

At the moment we are still trying to find out, but what we do know is that the immune system is split into two parts, the antibody response and the cell based response. The cell based response is further sub-divided into what is known as Th1 or Th2 biased responses. Infection with respiratory viruses has been shown to be a problem in asthmatics as these two sides of the cell based immune system may be unbalanced.

A mechanism to explain this unbalanced nature is that the Th1 and Th2 parts of the cell based immune system are mutually antagonistic. Th2 cells produce the cytokine IL-4 which blocks Th1 differentiation and Th1 cells produce IFN-? which blocks Th2 differentiation. Thus, individuals with an immune system skewed towards Th2, an asthmatic like myself a case in point, tend not to produce eosinophils and IgE-producing B cells. The relative lack of IFN-? limits the antiviral response and thus I become sicker.

In studies conducted at Imperial College London, in which they infected both healthy and asthmatic volunteers with rhinovirus, the virus caused significantly greater lower respiratory symptoms and reduced lung function in the asthmatics.

In these asthmatics virus multiplication was significantly related to lower respiratory symptoms, bronchial hyperreactivity and reductions in blood total CD8(+) lymphocytes. Lung function reduction was significantly related to the increase in inflammatory cell lower airway inflammation.

A key point is that virology and clinical outcomes were strongly related to deficient IFN-? and IL-10 responses and to augmented IL-4, IL-5, and IL-13 responses. Their studies have demonstrated increased virus-induced illness severity in asthmatics compared with normal subjects and provides evidence of strong relationships between virus load, lower airway virus-induced inflammation and asthma exacerbation severity. This indicates increased Th2 or reduced Th1 responses are likely important mechanisms.

Despite the hard work of the UK based world-renowned research group at Imperial College, we still do not fully understand the mechanism by which a simple common cold virus can cause such a serious illness in normally healthy adults.

At hVIVO (formerly Retroscreen Virology) we infect people with a respiratory virus such as Flu, Rhinovirus or Respiratory Syncytial Virus and quarantine them in a dedicated facility for up to two weeks. We do this to determine how the virus and the human body interact so that we can better understand the underlying mechanisms of the infection and thus develop:

  • diagnostics,
  • vaccines,
  • monoclonal antibodies
  • and antiviral drugs.

We have inoculated more than 2,100 healthy volunteers over the last fifteen years and have learnt some amazing things: now we intend to investigate further the effects of virus on asthmatics to better understand why that little virus causes them, and me, such a problem.

REFERENCES

Hindawi Publishing Corporation

Scientifica

Volume 2013, Article ID 405876, 12 pages

http://dx.doi.org/10.1155/2013/405876

Review Article

Rhinovirus-Induced Exacerbations of Asthma and COPD

Marc B. Hershenson

 

Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13562-7. doi: 10.1073/pnas.0804181105. Epub 2008 Sep 3.

Rhinovirus-induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production.

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