Rosa Rubicondior: Malevolent Design - How Zika Is Designed to Spread Maximum Suffering.

Illustration of Zika virus in blood

Kateryna Kon/Science Photo Library

Zika uses human skin as ‘mosquito magnet’ to spread virus further | LSTM

January was something of a joyous month for devotees of creationism's divine malevolence. Following closely behind the news of how it brilliantly designed HIV to use our cells defences against us so making it better at infecting and killing us, we have news of another breathtakingly brilliant design of a nasty little pathogen - the zika virus that causes microcephaly in children if their mothers become infected during pregnancy.

This news is that it turns our skin into a living 'magnet' to attract the vector that spreads it - mosquitos - so ensuring it gets transmitted to as many victims as possible. It does it by altering a gene and protein expression in dermal fibroblasts, causing the skin to produce odours that are attractive to mosquitoes. In effect, calling them to come and feed.

Before creationists start bleating unscientific and biologically non-sensical nonsense about 'genetic entropy' and devolution allowed by 'sin' I should point out that no mutation that conveys a benefit on an organism can be regarded as 'devolutionary'. It is classic evolution by natural selection. And, as per William Dembski's gibberish about 'specified complexity', any complex DNA or RNA sequence that codes for a specific function must be regarded as 'specified complexity', using his argument, so must have been specified by a magic designer, according to his misuse of statistics and probability. Or perhaps a creationist could explain why such a highly specific function of converting a human gene to make special mosquito-attracting scents, is not an example of Dembski's 'specified complexity'.

So, how was this, in creationist terms, intelligently designed virus, discovered to have this touch of brilliance in its design? That was the result if a new study by an international team led by Liverpool School of Tropical Medicine. Their findings are published, open access, in Communications Biology.

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).

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.

Zika is still spreading. Why don’t we have a vaccine yet?

Zika uses human skin as ‘mosquito magnet’ to spread virus further
Zika virus hijacks the skin of its human host to send out chemical signals that lure more mosquitoes to infect and spread the disease further, new research shows.
Zika transmission has been reported more than 90 countries as the spread of the Aedes aegypti mosquito that carries the virus, as well as dengue and chikungunya, has increased over recent years as an effect of climate change and urbanisation. Yet surprisingly little is known about the factors that drive Zika transmission success.

A new study led by Liverpool School of Tropical Medicine and published in Communications Biology shows that Zika causes metabolic changes in human skin that essentially transforms it from a protective barrier to a magnet for mosquitoes.

Their research shows that the Zika virus alters gene and protein expression in dermal fibroblasts, the cell type responsible for maintaining structural integrity in the skin. These metabolic changes increase the production of certain chemicals emitted through the skin, known as volatile organic compounds (VOCs), that are attractive to mosquitoes and encourage them to bite. Their findings are supported by an extensive meta-proteome analysis, a technique that examines the overall effect of the interaction of different types of gene and protein within an organism.

Our findings show that Zika virus isn’t just passively transmitted, but it actively manipulates human biology to ensure its survival. As Zika cases rise and Aedes mosquitoes expand their range, understanding the mechanisms by which they gain a transmission advantage could unlock new strategies for combating arboviruses. This could include developing genetic interventions that disrupt the signal transmitted through the skin which seems to be so attractive to mosquitoes. The possibilities are as intriguing as they are urgent.

Dr Noushin Emami, co-corresponding author Department of Molecular Bioscience
Wenner-Gren Institute
Stockholm University, Stockholm, Sweden
And Vector Biology Department (VBD)
Liverpool School of Tropical Medicine (LSTM)
Liverpool, UK.
Most Zika infections do not lead to disease, and those that do generally cause mild symptoms that last for 2-7 days.

Zika can occasionally cause more serious complications and can harm a developing baby if contracted by a pregnant woman.

This study was conducted in collaboration with Emami Lab at Stockholm University, alongside researchers from the Nature Research Centre in Vilnius, the University of Veterinary Medicine in Hanover, Molecular Attraction AB, Umeå University, Leibniz University Hannover, and the University of Greenwich.

Abstract
Transmission of Zika virus (ZIKV) has been reported in 92 countries and the geographical spread of invasive virus-borne vectors has increased in recent years. Arboviruses naturally survive between vertebrate hosts and arthropod vectors. Transmission success requires the mosquito to feed on viraemic hosts. There is little specific understanding of factors that may promote ZIKV transmission-success. Here we show that mosquito host-seeking behaviour is impacted by viral infection of the vertebrae host and may be essential for the effective transmission of arboviruses like ZIKV. Human skin fibroblasts produce a variety of metabolites, and we show that ZIKV immediately alters gene/protein expression patterns in infected-dermal fibroblasts, altering their metabolism to increase the release of mosquito-attractive volatile organic compounds (VOCs), which improves its transmission success. We demonstrate that at the invasion stage, ZIKV differentially altered the emission of VOCs by significantly increasing or decreasing their amounts, while at the transmission stage of the virus, all VOCs are significantly increased. The findings are complemented by an extensive meta-proteome analysis. Overall, we demonstrate a multifaceted role of virus-host interaction and shed light on how arboviruses may influence the behaviour of their vectors as an evolved means of improving transmission-success

Introduction
The human body comprises around 40 trillion (3.7 × 10¹³) cells¹, which produce an enormous variety of metabolites including volatile organic compounds (VOCs). The qualitative and quantitative changes in VOC profiles reflect the optimum status of healthy cells. The skin is the body’s largest organ, serving multiple essential functions, including acting as a physical barrier for protection, a site for sensory perception, and a centre for vitamin synthesis. The release of VOCs through the skin, which contributes to the distinct odours of the human body, is a familiar part of our daily experience². These VOCs include a large number of volatiles that can be listed as carboxylic acids, aldehydes, alcohols or ketones³. Dermal fibroblasts are the main cell type present in skin connective tissue (dermis)⁴. These mesenchymal/stromal cells derived from the embryonic mesoderm, reside in the dermal layer of skin. They produce extracellular matrix proteins to strengthen the dermal compartment and interact with epidermal cells⁵.

Zika virus (ZIKV) had not been widely known until a series of outbreaks occurred with severe clinical complications that made it a matter of global public health concern. The emergence of ZIKV followed a typical pattern of a vector-borne disease being introduced into a new ecosystem and host population and spreading rapidly with severe implications for human health. ZIKV is a mosquito-borne virus belonging to the genus Flavivirus and is transmitted to humans by mosquitoes of the genus Aedes. Both Aedes aegypti and Aedes albopictus are the primary vectors for ZIKV transmission in nature⁶. Vector-mediated transmission of ZIKV is initiated when a blood-feeding female Aedes mosquito injects the virus into the skin of its mammalian host, followed by infection of a wide range of permissive cells. Indeed, skin cells, including dermal fibroblasts were found to be permissive to ZIKV infection. Infection of skin fibroblasts rapidly resulted in the presence of high RNA copy numbers and a gradual increase in the production of ZIKV particles over time, indicating an active viral replication stage. In humans, the incubation period from mosquito bite to symptom onset is ≈3–12 days⁷. Accumulating data indicate that ZIKV alters the biochemical processes of the infected cells by modifying glucose^8,9 and fatty acid¹⁰ metabolism. However, no published data has yet revealed any changes in the composition of infected cell volatome. While Zhang and colleagues¹¹ demonstrated that flaviviruses can manipulate host skin microbiota to produce an odour that attracts mosquitoes, the specific role of infected human skin cells in manipulating mosquitoes’ behaviour remains unclear.

Mosquitoes have made themselves at home in new geographical regions throughout recent years, bringing with them some historically exotic diseases. Epidemiologic and laboratory studies have implicated various Aedes spp. mosquitoes as ZIKV vectors¹¹. In mosquitoes, it appears that the viral load is initially high on the day of feeding, but then decreases to undetectable levels for about ten days. After this incubation period, the viral content increases again by day 15 and remains high from days 20 to 60. This is important because it suggests that it takes about 10 days for the virus to reach the salivary glands of the mosquito where it can potentially be transmitted to humans⁷. There is currently no specific treatment or vaccine available to mitigate or prevent ZIKV infection. Prevention measures, particularly conventional vector control, are currently the priority while we await these and other advances in control of the substantial harm caused by this virus. The World Health Organization has issued recommendations on this matter¹².

To further understand this complex issue, this study aims to demonstrate how ZIKV manipulate vector behaviour by altering gene/protein expression in human dermal fibroblasts at different stages of infection. These changes lead to an increased release of mosquito-attractive VOCs, ultimately enhancing transmission success. Here, we describe how ZIKV infection of human host cells provoked the modified feeding behaviour of its tiger mosquito vector in a manner that plausibly results in enhanced transmission success.

Obviously, to creationism's intelligent designer who designed mosquitoes to drink human blood and so spread several nasty parasites and viruses, and gave them the ability to detect and home in on the scents we give off, it was a simple matter to design the zika virus to enhance those scents to attract more mosquitoes and have the virus spread as widely as possible, to maximise the number of children born with microcephaly. At least, since that is about all the zika virus does, we have to assume that wehoever designed it, designed it with that specific function in mind.

And William Dembski insists that whatever a DNA/RNA sequence produces it must have been intelligently specified to produce that outcome. The malice of this designer knows no bounds apparently. That's if you believe what creationists claim.

If you believe what science says, it's easy to see how genes mutating and being selected for when they convey an advantage can produce this sort of host-parasite arms race over time, especially if it only takes a few tweaks of the RNA sequence to manipulate one of our genes, and suddenly, lots more mosquitoes are homing in and spreading the new variant far and wide.

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