We modern humans often play petty blame game. It has become our habit to blame insects for our faulty life style!
It is true that Dengue is vector borne sickness. It is also true that certain protein in specific mosquito flag off the onset of dengue and other post-monsoon sicknesses. It is also reality that not all are afflicted by fever when mosquito bites!
What we see as Dengue epidemic, used to be Plague epidemic half a century back. Epidemics are natural and will happen time to time. It is natural way of population control.
During this sensitive time, it is our job to change diet as per season! Increase intake of certain diet and decrease/stop other as per season!
How do you feel when you see pictures from artificial famine of 1940s Bengal?
Disgusting right? Undercurrent of anger pass through entire body, resulted in shivering.
Our body cells go through similar famine trauma when we eat food (fast food, junk food, pesticide food) like morons, when we take unnecessary mental stress, when we indulge in sensual habits like animals. And that too during monsoon!
We are Churchill (who planned artificial famine in Bengal) for our body. On one hand we oppose subjugation by British and on the other hand, we blissfully enjoy same subjugation with own body! Worse breed of hypocrites? Yes, अनार्य, म्लेच्छा.
Roots of dengue or any viral infections are sown way back when we hamper our digestion. When we eat mindlessly against our prakriti, season and capacity of digestive fire (जठराग्नि).
It is actually a पित्त प्रकोप.
Here is the interesting research discussion why only selective few develop life-threatening dengue? It shows that the root is in the blood (पित्त) and not the vector transferred by mosquito!
Discovery helps explain why only some people develop life-threatening dengue infections
IgG antibodies to dengue enhanced for FcγRIIIA binding determine disease severity
A rare ability to enhance dengue virus disease
In some cases, secondary infections of dengue virus can be extremely serious and result in plasma leakage, thrombocytopenia, and hemorrhagic disease. This phenomenon has been attributed to antibody-dependent enhancement. Wang et al. show that a specific subclass of antibody, IgG1, which lacks fucosyl residues on the Fc segment of the heavy chain of the immunoglobulin, is elevated in patients with severe secondary dengue disease. These non-neutralizing antibodies bind activating Fc receptors and appear to cross-react with platelet antigens to cause platelet depletion, contributing to thrombocytopenia.
Dengue virus (DENV) infection in the presence of reactive, non-neutralizing immunoglobulin G (IgG) (RNNIg) is the greatest risk factor for dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). Progression to DHF/DSS is attributed to antibody-dependent enhancement (ADE); however, because only a fraction of infections occurring in the presence of RNNIg advance to DHF/DSS, the presence of RNNIg alone cannot account for disease severity. We discovered that DHF/DSS patients respond to infection by producing IgGs with enhanced affinity for the activating Fc receptor FcγRIIIA due to afucosylated Fc glycans and IgG1 subclass. RNNIg enriched for afucosylated IgG1 triggered platelet reduction in vivo and was a significant risk factor for thrombocytopenia. Thus, therapeutics and vaccines restricting production of afucosylated, IgG1 RNNIg during infection may prevent ADE of DENV disease.