African straw-coloured bat
OCD or Obsessive Compulsive Disorder is characterised by repeatedly and obsessively doing something which appears to have no aim, or at least an aim which isn't furthered by constant repetition.
Yet, when we look at biology, we see examples in great abundance of what would appear to be obsessive, constant repetition which actually achieves nothing, as though the designer is on some sort of mental treadmill and incapable of getting off it - assuming, that is, that you believe in a designer. This is not the act of a mentally healthy or intelligent being.
As though to illustrate this, we have an open access paper this week where the authors believe they have shown that bats and ebola viruses have been engaged in an arms race, possibly for 25 million years.
Abstract
Biological factors that influence the host range and spillover of Ebola virus (EBOV) and other filoviruses remain enigmatic. While filoviruses infect diverse mammalian cell lines, we report that cells from African straw-colored fruit bats (Eidolon helvum) are refractory to EBOV infection. This could be explained by a single amino acid change in the filovirus receptor, NPC1, which greatly reduces the affinity of EBOV-NPC1 interaction. We found signatures of positive selection in bat NPC1 concentrated at the virus-receptor interface, with the strongest signal at the same residue that controls EBOV infection in Eidolon helvum cells. Our work identifies NPC1 as a genetic determinant of filovirus susceptibility in bats, and suggests that some NPC1 variations reflect host adaptations to reduce filovirus replication and virulence. A single viral mutation afforded escape from receptor control, revealing a pathway for compensatory viral evolution and a potential avenue for expansion of filovirus host range in nature.
eLife digest
Ebola virus and other filoviruses can cause devastating diseases in humans and other apes. Numerous small outbreaks of Ebola virus disease have occurred in Africa over the past 40 years. However, in 2013–2015, the largest outbreak on record took place in three Western African nations with no previous history of the disease.
Human outbreaks of Ebola virus disease likely begin when a person encounters an infected wild animal. Though it remains unclear precisely which animals harbor Ebola virus between outbreaks, and how they transmit the virus to humans or other primates, recent work showed that some filoviruses do infect specific types of bats in nature.
Ng, Ndungo, Kaczmarek et al. sought to identify the genes that influence whether or not a type of bat is susceptible to infection by Ebola virus and other filoviruses. Several filoviruses, including Ebola virus, were tested to see if they could infect cells that had been collected from four types of African fruit bats. These bats are all found in areas where outbreaks have occurred in the past.
The tests revealed that a small change in the sequence of the NPC1 gene in some bat cells greatly reduced their susceptibility to Ebola virus. NPC1 encodes a protein that mammals need in order to move cholesterol within their cells. In humans, the loss of the protein encoded by NPC1 causes a rare but very severe disease called Niemann-Pick type C disease. This protein also turns out to be a receptor that the filoviruses must bind to before they can infect the cells. Further analysis then revealed that NPC1 has evolved rapidly in bats, with changes concentrated in the parts of the receptor that interact with Ebola virus.
Ng, Ndungo, Kaczmarek et al. went on to discover some changes in the genome sequence of Ebola virus that could compensate for the changes in the bat’s NPC1 gene. These findings hint at one way that a filovirus could evolve to better infect a host with receptors that were less than optimal.
Following on from this work, the next challenges will be to expand the investigation to include additional types of bats, other types of mammals, and other host genes that could influence filovirus infection and disease. Further studies could also examine the other side of the arms race – that is, the evolution of viral genes in bats. However, such studies would be complicated by the lack of viral sequences that have been collected from bats, because to date most have been isolated from humans and other primates instead.
https://doi.org/10.7554/eLife.11785.002
Introduction
Ebola virus (EBOV) and some of its relatives in the family Filoviridaef (filoviruses) cause sporadic outbreaks of a highly lethal disease. These outbreaks are thought to be initiated by viral spillover from an animal reservoir to a highly susceptible accidental host, such as a human or nonhuman primate (Feldmann and Geisbert, 2011; Leroy et al., 2005; Towner et al., 2009). Recent work suggests that some filoviruses infect bats in nature, and that these viruses may be distributed more widely than previously recognized. Very short RNA fragments corresponding to portions of ebolavirus genomes were detected in several frugivorous bats of the family Pteropodidae (‘Old World fruit bats’) in both Africa and Asia (Leroy et al., 2005; Jayme et al., 2015), and longer filovirus RNA fragments and near-complete RNA genomes were isolated from insectivorous Schreibers's long-fingered bats in Asia and Europe, respectively (Negredo et al., 2011.1; He et al., 2015.1). However, despite considerable efforts, infectious ebolaviruses have never been recovered from bats. By contrast, Marburg (MARV) and Ravn (RAVV) viruses were found to circulate in Egyptian rousettes (Rousettus aegyptiacus), indicating that these bats are susceptible to MARV/RAVV and encounter them frequently in nature. Egyptian rousettes have been proposed as natural hosts for these viruses (Amman et al., 2012; Towner et al., 2009). This progress notwithstanding, many key questions remain. For example, the biological factors that influence filovirus host range and interspecies transmission are still poorly understood, as are the virus-host relationships that determine which species of bats are susceptible to infection by EBOV and other filoviruses.
Viral entry receptors are key determinants of tissue tropism and host range (Radoshitzky et al., 2008; Sheahan et al., 2008.1; Hueffer et al., 2003; Demogines et al., 2013). Niemann-Pick C1 (NPC1), a highly conserved endo/lysosomal protein involved in cellular cholesterol trafficking, was recently identified to be an essential entry receptor for all known filoviruses (Côté et al., 2011.2; Carette et al., 2011.3; Miller et al., 2012.1; Ng et al., 2014). In this study, we uncover a pattern of virus and host species specificity in the filovirus susceptibility of bat cells, which can be explained by changes in the affinity of the essential interaction between NPC1 and the filovirus entry glycoprotein, GP. Crucially, genetic analyses reveal that NPC1 is under positive selection in bats, with a strong signature of selection at precisely the same residue that influences the filovirus-receptor interaction. Our findings suggest that amino acid sequence changes in NPC1 at these positively-selected sites represent host adaptations to resist filovirus infection, and reveal one pathway by which a filovirus could escape from receptor control. In sum, our results support the hypothesis that bats and filoviruses have been engaged in a long-term co-evolutionary relationship, one facet of which is a molecular arms race between the viral glycoprotein and its entry receptor, NPC1.
Melinda Ng, Esther Ndungo, Maria E Kaczmarek, Andrew S Herbert, Tabea Binger, Ana I Kuehne, Rohit K Jangra, John A Hawkins, Robert J Gifford, Rohan Biswas, Ann Demogines, Rebekah M James, Meng Yu, Thijn R Brummelkamp, Christian Drosten, Lin-Fa Wang, Jens H Kuhn, Marcel A Müller, John M Dye, Sara L Sawyer, Kartik Chandran.
Filovirus receptor NPC1 contributes to species-specific patterns of ebolavirus susceptibility in bats.
eLife, 2015; 4 DOI: 10.7554/eLife.11785
The ebola virus attacks host cells by attaching a glycoprotein on its surface to a receptor on the surface of host cells known as NPC1. However, in at least one species of bat, the African straw-colored fruit bat, a single amino acid change in the NPC1 receptor makes them immune to the ebola virus because it can no longer bind to their cells. However, a single amino acid change in the virus' glycoprotein can restore its binding ability.
From an analysis of NPC1 from 13 species of bat, the researchers believe they have detected evidence of rapid evolution in this receptor in bats, most likely caused by a rapid arms race between host and parasite. They have also shown that a fragment of the ebola virus genome became incorporated into bat genome some 25 million years ago which strongly suggests this arms race has been underway for at least that long.
If you don't believe in evolution and believe everything is intelligently designed, you have to believe your hypothetical intelligent (sic) designer keeps redesigning bats to make them resistant to EBOV and then redesigning EBOV so it can overcome resistance in bats. In 'intelligent (sic) design' terms there can be no other reason for this other than that the designer is carrying out a repetitive action for no ultimate purpose but appears to be unable to get off this treadmill.
Can any creationists suggest a better reason for these examples of arms races, which absolutely pervade the natural world, to no-one's ultimate benefit, other than the product of a designer with OCD?
With evolution, of course, evolution IS a treadmill from which living things cannot escape and so have no option but to repeatedly keep reacting to the here and now, because falling off that treadmill is called extinction. Evolution IS obsessive and compulsive because it is inevitable and has no intelligence, aim or plan. This is how we can tell it isn't being intelligently driven.
The Unintelligent Designer: Refuting The Intelligent Design Hoax
ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.
Available in Hardcover, Paperback or ebook for Kindle
The Malevolent Designer: Why Nature's God is Not Good
This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.
Illustrated by Catherine Webber-Hounslow.
Available in Hardcover, Paperback or ebook for Kindle
Illustrated by Catherine Webber-Hounslow.
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