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I've written recently about the lengths creationism's divine malevolence must have gone to to ensure one of its nasty little parasitic pathogens, the zika virus, gets to infect as many of its potential victims as possible. Science has now revealed how it then ensures as many babies being carried by its pregnant victims as possible are infected, by sneaking past the maternal/foetal barrier in the placenta.
Zika, is, of course, the mosquito-borne virus that causes microcephaly and associated mental handicap in babies whose mothers were infected during pregnancy.
To ensure the success of this method of increasing the suffering in the world, the designer had a major problem of its own making to overcome - it had given the human foetus a placenta that included a barrier between its circulation and that of the mother. This barrier is normally sufficient to prevent viruses crossing over into the developing foetus, so clearly, if an many children with microcephaly as possible are born, the designer had to find a way to bypass this barrier.
It produced the ingenious method of creating microtubules (small tunnels) between the mother's cells and the foetus's cells in the placenta and simply passing through them!
Unusually for creationism's divine malevolence, which normally behaves like a mindless evolutionary process and reinvents a novel solution for the same problem encountered by a different species, this is the same sneaky method used by a few other viruses to pass from cell to cell in a sheet of tissue, without going outside and making themselves available for the immune system to detect and respond to.
Tell me all about the zika virus, its evolution and recent spread, please. Zika virus (ZIKV) is a mosquito-borne flavivirus primarily transmitted by Aedes mosquitoes, particularly Aedes aegypti. First identified in 1947 in a rhesus monkey in Uganda's Zika Forest, it was subsequently detected in humans in 1952 in Uganda and the United Republic of Tanzania. (who.int).How it does so, is the subject of a research paper in Nature Communications by researchers from Baylor College of Medicine in collaboration with collaborators from Pennsylvania State University. Their research is explained in news item from Baylor College of Medicine.
Evolution and Lineages
Zika virus (ZIKV) is an RNA virus. Specifically, it is a positive-sense, single-stranded RNA virus belonging to the Flavivirus genus within the Flaviviridae family. Other notable flaviviruses include dengue, yellow fever, and West Nile viruses.
Because ZIKV has an RNA genome, it mutates and evolves more rapidly than DNA viruses, which may have contributed to its recent spread and ability to cause large outbreaks.
Phylogenetic studies have identified two main lineages of ZIKV: African and Asian. The virus remained relatively obscure for decades, causing only sporadic human infections in Africa and Asia. However, in 2007, a significant outbreak occurred on Yap Island in Micronesia, marking ZIKV's first major emergence outside its traditional endemic areas. (academic.oup.com)
The Asian lineage is particularly notable for its role in the outbreaks in the Pacific and the Americas. Genetic analyses suggest that mutations in the virus may have enhanced its ability to infect humans and spread more efficiently, contributing to its rapid dissemination. (frontiersin.org).
Global Spread and Recent Developments
Following the Yap Island outbreak, ZIKV caused significant epidemics in the Pacific, including in French Polynesia in 2013. In 2015, Brazil reported its first case, leading to a large outbreak associated with severe birth defects, such as microcephaly, and neurological disorders like Guillain-Barré syndrome. The virus then spread throughout the Americas, prompting the World Health Organization to declare it a Public Health Emergency of International Concern in 2016. (who.int).
As of May 2024, ZIKV transmission persists in several countries, though generally at low levels since 2018. Recent data indicate that three additional countries have reported autochthonous mosquito-borne transmission, and two more have established *Aedes aegypti* populations without documented ZIKV transmission. (who.int).
In January 2025, new research revealed that ZIKV can manipulate human skin to emit chemical signals attracting more mosquitoes, potentially facilitating further spread of the virus. (sciencedaily.com).
Prevention and Control
Preventing ZIKV infection primarily involves controlling mosquito populations and minimizing exposure to mosquito bites. This includes using insect repellent, wearing protective clothing, and eliminating standing water where mosquitoes breed. Given the association between ZIKV infection during pregnancy and birth defects, pregnant women are advised to avoid travel to areas with active ZIKV transmission. (who.int).
Despite ongoing research, there is currently no specific antiviral treatment or vaccine for ZIKV. Efforts to develop a vaccine have faced challenges, including fluctuating transmission rates and limited funding.
Stealth virus: Zika virus builds tunnels to covertly infect cells of the placenta
Infection with Zika virus in pregnancy can lead to neurological disorders, fetal abnormalities and fetal death. Until now, how the virus manages to cross the placenta, which nurtures the developing fetus and forms a strong barrier against microbes and chemicals that could harm the fetus, has not been clear. Researchers at Baylor College of Medicine with collaborators at Pennsylvania State University report in Nature Communications a strategy Zika virus uses to covertly spread in placental cells, raising little alarm in the immune system.
The Zika virus, which is transmitted by mosquitoes, triggered an epidemic in the Americas that began in 2015 and by 2018 had reached as many as 30 million cases. Understanding how Zika virus spreads through the human placenta and reaches the fetus is critical to prevent or control this devastating condition.
Professor Dr. Indira Mysorekar, co-senior author
Professor of medicine – infectious diseases.
Baylor College of Medicine.
The researchers discovered that Zika virus builds underground tunnels, a series of tiny tubes called tunneling nanotubes, that facilitate the transfer of viral particles to neighboring uninfected cells.
We discovered that the formation of these tiny tunnels is driven exclusively by a Zika protein called NS1. Exposure of placental cells to the NS1 protein of Zika virus triggers tunnel formation. As the tunnels develop and connect neighboring cells, a path opens for the virus to invade new cells.
Zika is the only virus in its family, which includes dengue and West Nile viruses among others, whose NS1 protein triggers the formation of tunnels in multiple cell types. Other viruses unrelated to Zika, such as HIV, herpes, influenza A and SARS-CoV-2, the virus that causes COVID-19, also can induce tiny tunnels in cells they infect and use the tunnels to spread to uninfected cells. This is the first time that tunneling has been shown by Zika virus infection in placental cells.
Dr. Rafael T. Michita, First Author Department of Medicine
Section of Infectious Diseases
Baylor College of Medicine, Houston, TX, USA.
Interestingly, the tiny conduits provided a means to transport not only viral particles, but also RNA, proteins and mitochondria, a cell’s main source of energy, from infected to neighboring cells.We propose that transporting mitochondria through the tunnels may provide an energetic boost to virus-infected cells to promote viral replication.
Long B. Tran, co-author
Department of Medicine
Section of Infectious Diseases
Baylor College of Medicine, Houston, TX, USA.
We also show that travelling through the tiny tunnels can potentially help Zika virus avoid the activation of large-scale antiviral responses, such as interferon lambda (IFN-lambda) defenses implemented by the placenta. Mutant Zika viruses that do not make tiny tunnels induce robust antiviral IFN-lambda response that can potentially limit the spread of the virus.
Dr. Rafael T. Michita.
Steven J. Bark and Deepak Kumar at Baylor College of Medicine and Shay A. Toner, Joyce Jose and co-senior author Anoop Narayanan at Pennsylvania State University are key members of the research team.
PublicationAltogether, we show that Zika virus uses a tunneling strategy to covertly spread the infection in the placenta while hijacking mitochondria to augment its propagation and survival. We propose that this strategy also protects the virus from the immune response. These findings offer vital insights that could be used to develop therapeutic strategies targeted against this stealth transmission mode.
Professor Dr. Indira Mysorekar.
Michita, R.T., Tran, L.B., Bark, S.J. et al.
Zika virus NS1 drives tunneling nanotube formation for mitochondrial transfer and stealth transmission in trophoblasts.
Nat Commun 16, 1803 (2025). https://doi.org/10.1038/s41467-025-56927-2
AbstractIt goes without saying that we can exclude Michael J. Behe's valiant attempt to absolve creationism's god of any culpability by blaming 'sin' or rather the alleged 'genetic entropy' 'sin' allows with resulting 'devolution' [sic], because any mutation which benefits the virus is evolutionary and can't logically be presented as a lessening of some assumed initial design perfection. As for William A. Dembski, his assertion that 'complex specified information' proves intelligent design, then why would the 'complex specified information' that gives ZIKAV this ability be excluded?
Zika virus (ZIKV) is unique among orthoflaviviruses in its vertical transmission capacity in humans, yet the underlying mechanisms remain incompletely understood. Here, we show that ZIKV induces tunneling nanotubes (TNTs) in placental trophoblasts which facilitate transfer of viral particles, proteins, mitochondria, and RNA to neighboring uninfected cells. TNT formation is driven exclusively via ZIKV non-structural protein 1 (NS1). Specifically, the N-terminal 1-50 amino acids of membrane-bound ZIKV NS1 are necessary for triggering TNT formation in host cells. Trophoblasts infected with TNT-deficient ZIKVΔTNT mutant virus elicited a robust antiviral IFN-λ 1/2/3 response relative to WT ZIKV, suggesting TNT-mediated trafficking allows ZIKV cell-to-cell transmission camouflaged from host defenses. Using affinity purification-mass spectrometry of cells expressing wild-type NS1 or non-TNT forming NS1, we found mitochondrial proteins are dominant NS1-interacting partners. We demonstrate that ZIKV infection or NS1 expression induces elevated mitochondria levels in trophoblasts and that mitochondria are siphoned via TNTs from healthy to ZIKV-infected cells. Together our findings identify a stealth mechanism that ZIKV employs for intercellular spread among placental trophoblasts, evasion of antiviral interferon response, and the hijacking of mitochondria to augment its propagation and survival and offers a basis for novel therapeutic developments targeting these interactions to limit ZIKV dissemination.
Michita, R.T., Tran, L.B., Bark, S.J. et al.
Zika virus NS1 drives tunneling nanotube formation for mitochondrial transfer and stealth transmission in trophoblasts.
Nat Commun 16, 1803 (2025). https://doi.org/10.1038/s41467-025-56927-2
Copyright: © 2024 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Of course, both Dembski's and Behe's assertions are simple attempts to deny that evolution is the mechanism by which parasitic arms races, of which this ability of the ZIKAV is the result, result in these sorts of pathogens and the suffering they cause. Behe's excuse fails because of its utter biologically nonsensicality, and Dembski's assertions walk straight into the trap of contradicting Behe while making his designer look entirely responsible for parasites and the suffering they cause, contrary to Christian claims that their designer god is omnibenevolent.
These Deception Institute fellows have tied themselves in knots trying to avoid admitting that evolution is the logical explanation for parasites and made fools of themselves in the process.
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