I am on vacation, on this Christmas day of 2014, sitting by the beautiful, blue Caribbean sea with no plan to work or write here, that I read an article in “Scientific American” on “Haemophilia”. The article classifies this coagulating deficiency disease into congenital and acquired, while by congenital it means genetic as it is known for long in medicine! The genetic variety of the disease as it is well known, is a chromosome X-linked recessive trait that passes to male offsprings, while the women or the mothers are the asymptomatic carriers. To many and to me for long this has been a non-debatable genetic disease with no association with environmental factors including infections and insults by micro-organisms like so many other diseases such as cancers and autoimmune disorders as written in the articles of this website! In wonder of finding out of any such association (s) as I have already come to believe that genetics in pure sense has either a very minimal role in causing diseases or none, I had to spend some time of my vacation on search for this truth!

 Accidentally, Haemophilia type B that is caused by a mutation of the coagulation or clotting factor IX gene that leads to a deficiency of clotting factor IX and It is the second-most common form of haemophilia after haemophilia A, and used to be called “Christmas disease”! This genetic disease is not related to the Christmas day, the day that I am writing this post, but rather named after Stephen Christmas, the first patient who was described with this disease. Again ironically Hepatitis B caused by Hepatitis B virus antigen (HBsAg) has for long been identified in some haemophiliacs, while asymptomatic for hepatitis. This antigen that is also referred to as Australia Antigen (Au-ag), discovered by Nobel prize winner, Baruch Blumberg in an Australian aboriginal person, and has been well recognized and reported of ability to cause long-term damages to the humans, beyond an acute hepatitis!

 While all types of hepatitis including the common three, A, B and C could cause long-term disease repercussions, such as hepatic cancer by Hepatitis C Antigen (HCsAg), and attack through our sex or X-chromosome by hepatitis B virus and its HBsAg , causing diseases such as Haemophilia that still by many including experts and scientists in the field being thought as purely genetic. This is while some such as A.P. Waterson more than 42 years ago in 1972, has alarmed us so elegantly about such long-term impact by the microorganism world : “To the patient and his doctor the typical virus infection is short in incubation, acute in course, and rapid in its progress to death or immunity. However, so far as the virus is concerned this arrangement is not necessarily either the optimum or the norm. It is not the optimum because no virus seeks host organisms which are dead or clinically immune….it is true that classical virus infections such as measles, rubella, varicella,…or viral hepatitis manifest themselves typically with such an illness, but for more than a hundred years it has been recognized, particularly by veterinarians, that some infections may be more prolonged in their course…”

With the huge epidemic of viral hepatitis, an estimated 350 million individuals infected worldwide with type B and about 90% of children in the developing world being infected with type A by age 10 and apparently immune by adulthood, but asymptomatic carriers of the virus, our livers seem to be the optimum medium for this virus to live through us until our final day of demise on the earth. While other viruses, e.g. Epstein Barr Virus (EBV) and Coxsackievirus cost us autoimmune disorders and cancers, by affecting our genetic make up, the hepatitis viruses get through our sex or X-chromosome to infect us for ever and makes us believe that some diseases such as Haemophilia are purely genetic. 

Genes like alphabetical letters or computer programming, are only means of transcription and transmissions of our traits and not causes of diseases! No living thing would cause its own demise and produce diseases to itself! Mutations in the genes that cause diseases do not happen as random, as it is still currently thought so, but by exogenous offenders, such as bacterial and viral insults that have been cited elsewhere in the other posts of this website. In case of Haemophilia, as an example of being thought to be purely genetic, first of the infected x-chromosome is only passed on to the males, while the females including the mothers could be only carriers. Genetic mutation to cause this disease has not happened by random and by fault, but by viruses such as hepatitis B and C that after an apparent or masked brief and acute infection have remained in the body of the mother carriers or the father victims (as acquired haemophilia) to pass it on to the next generations through sitting on our x-chromosome! Now Isn’t the time to appreciate the damage by the microorganism world and reveal the answer to the ancient “chicken or egg” or “genetic or environment” dilemma once for all! Yes that it true, despite our denial to accept , it is all microbial (viral or bacterial) if not physical insults or traumas and not pure genetic!  

  Refrences:

• Showraki, Mostafa.  “A new look at Cancer”. medicinerevisited.com.
• Showraki, Mostafa.  “A new look at infections”. medicinerevisited.com.
• Showraki, Mostafa.  “Trauma and insults”. medicinerevisited.com.
• Showraki, Mostafa.  “Breast Cancer:Revisited”. medicinerevisited.com.
• Showraki, Mostafa.  “Ovarian and endometrial Cancers:Revisited”. medicinerevisited.com.
• Showraki, Mostafa.  “A new look at the prostate cancer”. medicinerevisited.com.
• Showraki, Mostafa. “Viral attacks”. medicinerevisited.com.
• Biggs R, Douglas AS, MacFarlane RG, Dacie JV, Pitney WR, Merskey C, O’Brien JR (1952). Christmas disease: a condition previously mistaken for Haemophilia.
• Waterson AP. Host-virus relationships with special reference to Newcastle disease and serum hepatitis. J Clin Pathol Suppl (R Coll Pathol). 1972; 6: 1–7.
• van Lunzen J, Altfeld M. Sex differences in infectious diseases-common but neglected. Infect Dis. 2014 Jul 15;209 Suppl 3:S79-80.
• Yue M, Feng L, Tang SD, Wang JJ, Xue XX, Ding WL, Zhang Y, Deng XZ. Sex-specific association between X-linked Toll-like receptor 7 with the outcomes of hepatitis C virus infection. Gene. 2014 Sep 15;548(2):244-50.