In the mid 1990’s when most of our results from the Central Queensland Indigenous Cardiac Risk Factor Study were available, I contacted and discussed the Cytomegalovirus results with Sir Gustav Nossal. He wrote and indicated that there was interest in a vaccine amongst the Infectious Disease people and Paediatritians to help avoid the neonatal and child infections, that frequently had lingering and limiting neurological side effects.
In this instance we had an Indigenous Australian cohort with known extensive CHD, that died near 20 years prematurely from the same, that were universally and heavily infected with Cytomegalovirus that was arguably the most likely involved infectious agent in CHD, from research evidence to date.No we had no proof of causation, but the associations seemed too many to be coincidences.My thesis was that Cytomegalovirus was the ‘injury agent’that may have initiated the first endothelial insult, the genisis of fatty steaks and fibrous plaques.The next stages that birthed the atheroma lesions were determined by life practices and nutrition, that were not an issue in the young. The early lesions found in fetus’s, neonates and children were later found in young and older adults. Too many in cardiology reluctantly with time, accepted these lesions as prototypes for the mature atheroma lesions.
So the patient Cytomegalovirus infectivity increased over the last century, a mirror image of the prevalence of CHD? Not so, nor did it have to. This ubiquitous virus in the affluent and non-affluent populations, increased with age and infection varied in different populations, but there were patterns. Those in poverty and low socio-economic groups had the highest infectivity rates. In our study, all studied from 4-64 years were seropositive. So this cohort theoretically were potential candidates to effect initial injury with Cytomegalovirus, according to my thesis. If they did, their life practices of smoking, alcohol and CHO laden nutrition with sugar and trans fats created a status of insulin resistance, inflammation and Athrogenic Dyslipidemia, which is the primary source of small dense oxidised LDL found commonly in atheroma lesions, precisely what we found in our Indigenous Australian Study!! Saturated fat and cholesterol had nothing to do with this, because this population were low consumers of the same. I treated 367 with a fibrate with this dyslipidemia.Their mean LDL and total cholesterol were within near normal limits. I have since reviewed many Indigenous diabetic studies and found their lipid results were similar, with normal or near normal total cholesterol, LDL levels with TG and HDL indices consistent with Atherogenic Dyslipidemia.These were older studies and the authors were not aware of the cardiological significance of these results.Many cardiologists were’nt either!!
At the time I discussed the possibility of a vaccine with Sir Gustav Nossal, we both realised it was technically a way off and the evidence to use it to avoid CHD was not compelling. That was in 1997:Is the situation different now?I believe it is. The US in the last 20 years has developed three different’types’ of vaccine and have reached trials in humans. Results to date are troubled with potency and time of effectiveness as well as biological design, which is complicated. It is still very early days, but there is an active movement in the US to eliminate the infection in the young, which has been estimated to cost two billion dollars a year there. If vaccination became common, ubiquitous, we could see another study play out with CHD perhaps. Selecting the sexually mature teenager potentially could reduce infection in the individual and infection transfer to their progeny.
At this stage, irrespective of Cytomegalovirus infection, the metabolic changes that arise with CHO overdosing, smoking, food processing need to be attended to and vaccination could be a bonus to help reduce, eliminate atheroma and CHD, particularly amongst the known susceptible. I should emphasise at this stage we have another species model in the chicken with another similar virus, not a human. But if the Americans produce an acceptable effective vaccine in the next decade to avoid the neurological damage of blindness, deafness and intellectual deficit in the new born, with time we may see if the virus contributes, initiates the early atheroma lesions.