Engorged Tick"
Timothy Takemoto / Flickr cc
One of the problems with claiming that biological complexity proves intelligent design is that the argument cannot stop conveniently at butterflies, flowers and the human eye. If complex biological machinery requires a designer, then the same reasoning must apply to parasites and pathogens. A virus’s ability to infect us cannot become an unfortunate accident merely because crediting the supposed designer would now be embarrassing. Nor can the animal that carries it from host to host be excluded from the reckoning.
A newly identified tick-borne virus in China provides another uncomfortable example. Described in a correspondence in The New England Journal of Medicine, Asian longhorned tick nairovirus, or ALTNV, is associated with fever, fatigue, gastrointestinal symptoms and, in some patients, reduced platelet counts. Its vector is the already familiar Asian longhorned tick, Haemaphysalis longicornis; experiments demonstrated transmission to mice. “New” here means newly recognised by science, not shown to have come into existence recently.
The clinical findings deserve care. All 56 patients reported with ALTNV alone recovered without lasting effects. However, seven of 38 patients infected with both ALTNV and Dabie bandavirus died. These deaths do not establish that ALTNV alone is lethal, or determine its contribution to the fatalities. They do place the discovery within a system of tick-borne infections capable of causing serious illness and death.
Now apply the creationist rule that functional complexity and genetic information require an intelligent author. On that premise, the designer must take responsibility for the infectious agent and its means of delivery. Here is a blood-feeding animal whose activities provide a route for viruses to enter other animals, including humans. If every relevant adaptation was knowingly intended by an all-knowing creator, then the resulting suffering cannot be dismissed as an unforeseen side-effect. The alleged designer knew what its creations would do.
That is the force of the malevolent-designer argument. It does not require us to believe that a supernatural intelligence actually makes viruses. It asks why features that serve pathogens should count as evidence of loving craftsmanship when equivalent features serving their victims are routinely presented as precisely that. If the designer receives credit for our defences, it must also answer for the threats those defences sometimes fail to overcome. Deliberately creating the means of making people ill is hardly an obvious expression of benevolence.
For the abundant natural evidence that, if the ID advocates' claims are true, their designer is a malevolent genius, not the omnibenevolent creator they would have people believe, read:
The Malevolent Designer: Why Nature's God is Not Good
Evolution requires no such moral contortions. Natural selection has no concern for our comfort, and adaptations that favour one organism need not benefit another. Human suffering is neither its objective nor something it works to prevent. But once ID advocates replace that indifferent process with deliberate, informed intention, they create their own theological difficulty: the same “proof” that supposedly reveals a benevolent designer also implicates that designer in the machinery of disease.The Malevolent Designer: Why Nature's God is Not Good
How ticks transmit viruses — and why coinfection matters. Ticks are blood-feeding arachnids, related to mites rather than insects. Their feeding habits connect them with a succession of animal hosts, creating opportunities for pathogens to move between those hosts. The Asian longhorned tick, Haemaphysalis longicornis, is an established species; it is the identification of another virus it can transmit that is new.The research was also covered in a news report from the University of Minnesota’s Center for Infectious Disease Research and Policy (CIDRAP).
More than a contaminated needle
A feeding tick anchors its mouthparts in the skin and takes a blood meal. Its saliva helps it feed and can contain substances that reduce the host's awareness of the bite. If the tick carries a transmissible pathogen, saliva entering the bite site can introduce that pathogen into the host. Conversely, feeding on an infected animal can allow a tick to acquire an infection.
A biological vector is more than something with contaminated mouthparts: it supports part of the pathogen's life cycle. Whether a particular tick species can transmit a particular virus depends on their biological compatibility. Finding viral material in a tick does not, by itself, demonstrate that the tick can pass on an infectious virus.
How an infection can persist
Hard ticks develop through four stages: egg, larva, nymph and adult. Two different mechanisms can help a pathogen persist in a tick population:
These mechanisms are not universal to all tick-borne pathogens. For Asian longhorned tick nairovirus (ALTNV), the researchers demonstrated both experimentally, as well as transmission from H. longicornis to mice.
- Transstadial transmission: an infection survives the tick's moult from one developmental stage to the next. The same individual remains infected as it develops.
- Transovarial transmission: an infected female passes a pathogen to her offspring through her eggs. The infection crosses from one generation to another.
Why more than one pathogen matters
The same tick species can transmit different pathogens. An individual tick carrying multiple transmissible pathogens may pass on more than one infection during feeding, although a patient can also acquire separate infections from separate bites. Finding two infections in one patient does not establish that both came from one tick.
ALTNV and Dabie bandavirus share a tick vector. In this study, patients infected with both had respiratory symptoms and kidney impairment more frequently than those infected with Dabie bandavirus alone. Seven of the 38 coinfected patients died, whereas all 56 patients reported with ALTNV alone recovered without lasting effects. The findings do not establish that ALTNV alone caused the deaths.
Discovery is not a creation date
A newly identified virus may have circulated unnoticed before scientists developed the means to recognise it. Its discovery date tells us when it entered scientific knowledge, not when it first evolved.
Brief glossary
- Vector
- A living carrier, such as a tick, that transmits a pathogen between hosts.
- Host
- An organism in or on which a parasite or infectious agent lives.
- Pathogen
- A biological agent, such as a virus or bacterium, capable of causing disease.
- Zoonosis
- An infection naturally transmissible between non-human vertebrate animals and humans, sometimes through a vector.
- Coinfection
- Infection of the same host with more than one infectious agent at the same time.
Scientists in China discover new tick-borne virus that causes flu-like illness
Scientists in China have identified a novel tick-borne virus that causes an influenza-like illness characterized by fever, fatigue, gastrointestinal (GI) symptoms, and abnormal lab findings.
The team, led by researchers from the State Key Laboratory of Pathogen and Biosecurity in Beijing, has designated the new orthonairovirus as the Asian longhorned tick nairovirus (ALTNV).
Their discovery, published yesterday in the New England Journal of Medicine, stemmed from a probe into why 30% of patients with signs and symptoms of infection with Dabie bandavirus (DBV) test negative for the tick-borne hemorrhagic fever.
Severe fever, low platelet count
DBV disease, which causes severe fever with thrombocytopenia syndrome (SFTS), is found throughout Asia and has a case-fatality rate of 10% to 30%. Thrombocytopenia is a low platelet count. The World Health Organization lists DBV as a priority for research.
The team obtained samples from patients bitten by ticks at sentinel hospitals in parts of China where tick-borne viruses circulate. The researchers identified the new virus through RNA sequencing and viral isolation.
The cocirculation of ALTNV and DBV in the same areas, coupled with their shared tick vector, underscores the need for improved differential diagnosis between infections with these viruses in regions where SFTS is endemic.
Phylogenomic analyses identified ALTNV as an orthonairovirus in the family Nairoviridae that shared under 80% of the amino acids in other species in the genus.
Inoculation of cells with ALTNV RNA–positive human serum resulted in growth of a virus identified via immunofluorescence of viral antigen as ALTNV. Characteristics of orthonairoviruses were also seen on electron microscopy, and viral replication was detected in multiple cell lines.
15% of DBV-negative patients had ALTNV
Of all 3,163 patients tested, 10.4% were positive for ALTNV based on detection of RNA or immunoglobulin M antibodies. Among patients who tested negative for DBV, 15.1% tested positive for ALTNV.
The most common manifestations of infection with ALTNV alone were fatigue (84%), GI problems (80%), thrombocytopenia (38%), and elevated aminotransferase concentrations (indicating inflammation or injury of the liver or other tissues; 36%). These patients recovered completely.
Relative to infection with DBV alone, coinfection with ALTNV and DBV (38 patients) was linked to higher rates of respiratory symptoms (61% vs 38%) and kidney impairment (84% vs 66%). Seven (18.4%) coinfected patients died.
ALTNV RNA was detected in 1.3% of 47,428 ticks in 15 provinces, with the highest prevalence in Haemaphysalis longicornis ticks (1.8%). Experiments showed that H longicornis can transmit the virus to mice.
Publication:
The difficulty for intelligent design advocates is one of consistency. If biological machinery is evidence of deliberate design when it benefits us, the same argument must apply when it benefits a pathogen at our expense. They cannot credit their designer with the immune system while treating the infectious agents it struggles against as someone else’s responsibility. On their own premise, both sides of the conflict belong to the same supposed creative intelligence.
This does not mean the discovery of ALTNV proves the existence of a malevolent god. It exposes the consequences of inserting an all-knowing designer into an explanation that requires no such being. If the capacity to infect, persist and spread was deliberately supplied, then the resulting suffering was foreseeable. Describing that arrangement as the work of a benevolent creator requires an additional theological excuse; it does not follow from the biology.
Nor does invoking “the Fall” explain how a virus acquires the molecular machinery needed to exploit its hosts. If natural processes can produce such functional adaptations, the claim that these require intelligent intervention loses its force. If the designer supplied them instead, responsibility returns to the designer. Calling disease a punishment merely changes the proposed motive for causing suffering.
Evolution presents no equivalent contradiction. Selection can favour successful transmission without foresight, concern for human welfare or any intention to cause disease. The researchers, meanwhile, have done something demonstrably useful: identified a previously unrecognised infection and clarified a problem for diagnosis. Whatever comforts intelligent design offers its advocates, understanding pathogens and reducing their harm depend on investigating nature, not assigning its workings to an inscrutable plan.
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