Microcephaly is a disorder in the development of the nervous system, resulting in restricted brain (and skull) growth. It manifests either prenatally or after birth (in the baby’s first years) and is attributed to various factors (usually, nowadays, genetic, such as damage to a chromosome). It is an old disease and had not been associated with the Zika virus until recently.
The Zika virus, on the other hand, has been known since the 1950s and is considered responsible for the transmission of dengue fever, yellow fever, as well as a form of encephalitis. This (Japanese encephalitis) is caused by a virus (Japanese encephalitis virus) that is transmitted by two species of mosquitoes that are endemic in eastern and southeastern Asia (less so in sub-Saharan Africa): Culex tritaeniorhynchus and Culex vishnui – for the curious. Given that the Zika virus, which first appeared some years ago in the Caribbean (and from there began to spread to Central and South America), belongs to the African subgroup of the virus, its association with cases of microcephaly seems to hold, from a “historical” perspective. However, there are also estimates that attribute its American emergence to its Asian strain.
In any case, the recently known cases of Zika infection reported mild to very mild symptoms of a moderate form of dengue fever, symptoms that were treated with rest. Even if, retrospectively, the virus can be associated with causing some form of encephalitis, the massive outbreak of such side effects alone, in 2015, is a serious issue. And not only from a social perspective…
A very recent publication (late November 2015) of research on the “genetic identity” of Zika in its recent, particularly devastating appearance1, attributes the fact (not the mass encephalopathies in embryos but) that it is easily transmitted from human to human (and, consequently, from pregnant women to embryos), to a “change” in the composition of one of its RNA bases. If we are not mistaken, such changes are called mutations.
And here begin questions that are unlikely to be answered in a way that is so “straightforward” as to leave no serious suspicions. Genetic mutations (of specific viruses) are possible in a “natural” way, anyway. However, in the case of the increased pathogenicity of Zika in embryos, as well as its transmissibility from human to human (which was not happening before), a “non-natural” event intervenes. In 2011, the small British biotechnology company Oxitec sold to the Brazilian government a genetically modified mosquito (of the Aedes aegypti species), which had an additional “killer” gene that “killed” the eggs (of the species), so that the mosquito population in Brazil would gradually decrease, and thus the risk of transmitting dengue fever… in view of the Olympic Games, in the summer of 2016, in Rio de Janeiro.
Is it possible that the genetic mutation of the Zika virus host (the mosquito) caused a mutation in the virus itself? The usual process of “jumping” DNA segments from one organism to another (and in this case from the mosquito to the virus) does not apply here, since Zika does not have DNA. However, the research we mentioned earlier identifies a “change” in the Zika’s RNA that is not “borrowed” DNA from humans (other hosts) but rather an adaptation to the “host” environment in order to improve the “circulation of the virus.” Such a process is natural, since every living species (and the viruses within them) biologically “deal” with how they will survive and multiply.
It is a complex and unpredictable process of “interactions” between living organisms, which does not refer to the narrow version of genetic material exchange. Therefore, the question we formulated earlier (and possibly others are formulating at this moment, here and there on the planet) can be specified as follows: is it possible that the significant reduction of the Zika “natural” host (the Aedes aegypti mosquito) caused a mutation of it in such a way as to “exploit” better another host, the host-human, and from this “change” was also caused its high pathogenicity;2
Given that the actual knowledge of geneticists (including those specializing in mutations) is neither as extensive nor as solid as they advertise, the above question represents a possibility that cannot be theoretically ruled out; and it will take a very long time to confirm or exclude it in a “scientific” way.
Until then, however, the “coincidence” of a genetic mutation of a mosquito and its mass “release” into the natural environment (in Brazil in 2011) and the appearance in the same environment a few years later (in 2015) of a particularly virulent version of the Zika virus (for the elimination of which the mosquito’s mutation was supposedly carried out) leaves many, far too many, margins. Either for “conspiracy theories” or for something more solid: reasonable and serious reservations about the consequences of dispersing laboratory genetically modified organisms.
Although no one would accuse Oxitec of doing it “on purpose,” the concerns and questions surrounding the mass outbreak of microcephaly in embryos in Latin America (for now…) due to Zika threaten to become a tombstone for one of the most dynamic industries of the new capitalist model: biotechnology. The money and interests are many and large. Billions… And they will do everything possible (propagandistically) to disconnect the genetic mutation of the mosquito and microcephaly.
we may never (and how validly?) learn whether the specific “survival” mutation detected in Zika’s RNA is the only one or if there are others; and whether one or more of them could be associated with the microcephaly epidemic. We consider this highly unlikely.
We do not have a crystal ball!!! However, the case of the Zika virus, apart from being yet another mass fear used to control proto-cosmic societies3, has serious chances of already being the “Thalidomide scandal” of modern biotechnology….
- Spread of the pandemic Zika virus lineage is associated with NS1 codon usage adaptation in humans. ↩︎
- According to the research we are referencing (from molecular biologists…), the “defense” mechanism of Zika virus RNA, as is generally the case with viruses, is to “spy on” and “copy” segments of the host’s DNA, particularly those that activate its immune system, in order to mutate more effectively and enhance its own survival and replication capabilities. This specific research identified mutations in the virus’s genes, designated as NS1 and NS4A, which, according to the researchers, are associated with the virus’s ability to be transmitted from the (pregnant) mother to the embryo—something that did not occur previously. The findings are supported by data indicating that these particular mutations are incompatible with the DNA of the Zika virus’s “historic” host, the Aedes aegypti mosquito—and are unrelated to the virus’s survival within mosquitoes.
What is noted is that the high pathogenicity of Zika (plus…) is due to acquiring the ability to be transmitted to embryos. What the research does not address (because it was beyond its scope) is whether this specific mutation is also responsible for blocking the neurological development of embryos, leading to microcephaly…. ↩︎ - Sarajevo no 102, January 2016, management by stress. ↩︎