Nematodes are famous because of their parasitic members, which do not only parasitize animals but also plants. People that deal with gardening or agriculture may know that sometimes a plant becomes sick because of “nematodes”.
A genus of nematodes that is commonly associated with grapevines is Xiphinema, whose species are known as dagger nematodes. The two most widely studied species are Xiphinema americanum, the American dagger nematode, and Xiphinema index, the California dagger nematode, but during the last decades it became clear that those species are actually a complex of very similar species and new ones are constantly been described. One of them, described in 2016, is Xiphinema browni, which I decided to call Brown’s dagger nematode. It was named after the nematologist Derek J. F. Brown.
Brown’s dagger nematode was found associated with the roots of grapevines and apple trees in Slovakia and the Czech Republic. Among 86 identified females there was only one male, indicating a huge disparity in sex ratios and the probability that females are parthenogenetic, i.e., they can lay fertile eggs without being fertilized by a male. Females measure up to 2.5 mm in length and the only known male measured 1.8 mm.
Female (left) and male (right) of Xiphinema browni. Modified from Lazarova et al. (2020).*
Since Brown’s dagger nematode was found associated with grapevines, its life cycle is likely similar to that of most other dagger nematodes. Adults are external parasites of grapevine roots and eventually of other woody plants. They live on the root surface and use their long odontostyles (a needle-like proboscis) to perforate the roots and suck the content of their vascular tissue. As a reaction, the plant produces swollen club-like galls on the root tips. The root then branches behind the swollen tip, only to be attacked again, developing another gall and having to branch again. This starts to weaken the plant, which can compromise grape production.
Anterior end of a female with the odontostyle slightly exposed. Modified from Lazarova et al. (2020).*
Females lay their eggs scattered through the soil, not forming clusters, and juveniles pass through about 4 stages in the soil before turning to the parasitic mode.
As another grapevine-feeding dagger nematode, Brown’s dagger nematode is probably also a vector of the grapevine fanleaf virus, which is transmitted to grapevines by the California dagger nematode. This happens when the nematode feeds on an infected plant and then moves to a healthy plant, carrying the virus with it. Grapevine fanleaf causes chlorosis (loss of chlorophyll) and distorts the leaves, making them look like fans, hence the name. As you can imagine, the poor plant becomes even weaker than it already was due to the nematodes sucking it. This can be a nightmare to vineyard owners.
The grapevine fanleaf virus can be a devastating disease for grapevines but in the nematode’s body it seems to have benefitial effects, increasing the survival of these small roundworms. Perhaps this stimulates the dagger nematodes to spread it further, in a sort of “evil coalition”.
Lazarova S, Peneva V, Kumari S (2016) Morphological and molecular characterisation, and phylogenetic position of X.browni sp. n., X.penevi sp. n. and two known species of Xiphinemaamericanum-group (Nematoda, Longidoridae). ZooKeys 574:1–42. https://doi.org/10.3897/zookeys.574.8037
Two mosquitoes of the genus Aedes, Aedes aegypti and Aedes albopictus, are invasive species in tropical and subtropical regions worldwide. While A. aegypti is native from Africa, A. albopictus is originally from southeast Asia, but both species have been spread by humans and continue to increase their range.
Both species are known as vectors of several diseases that affect humans, especially those caused by Flavoviruses, which include the Yellow fever, Dengue fever and Zika fever. Chikungunya, caused by a species of Alphavirus is also transmitted to humans by them. Moreover, they can also transmit some nematodes, such as the heartworm that infects the heart of dogs and other carnivores.
Aedes aegypti biting a human and having a delicious bloody meal. Photo by James Gathany.
Because A. aegypti and A. albopictus pose such a huge threat to public health, getting rid of them is top priority. Here in Brazil, there is a massive national campaign to reduce the ability of Aedes to reproduce by avoiding containers with still water in the open, such as flower vases, buckets, uncovered barrels, discarded tires and virtually everything that can retain water long enough for the larvae to develop. I have to say, though, that this all seems to be useless. The mosquitoes continue to spread and the cases of dengue fever continue to grow. The fact is that the mosquitoes will find a place to lay their eggs. If they don’t find it in your backyard, they will find it in the forest or any vacant lot.
Instead of forcing them to lay their eggs where we cannot see, we should stimulate them to lay their eggs around us and then kill the larvae. Several aquatic predators have been tested as potential allies, including larvivorous fish, dragonfly nymphs, copepods, planarians and even other mosquitoes whoses larvae eat the larvae of Aedes! The use of these predators showed mixed results. Larvivorous fish are difficult to maintain in water tanks at home and dragonfly nymphs are too generalist as predators.
Now a new predator has been suggested: a plant! Yes, a carnivorous plant of the genus Utricularia, which includes species known as bladderworts. These aquatic plants have little bladder-like structures that function as traps to capture small animals. The bladder is hollow and has an internal negative pressure in relation to the environment surrounding it. This negative pressure is created by water being constanly pumped out of the bladder through its walls via active transport. The bladder’s opening is covered by a small lid that avoids water to fill it again when the trap is set. Surrounding the lid, there is a group of bristle-like protuberances. When an animal is moving through the water and moves one of those bristles, they slightly deform the lid, breaking the seal and allowing water to enter the bladder. The negative pressure then sucks water quickly into the bladder, dragging the small animal with it. Then it is only a matter of time for the poor animal to be digested.
Watch the plant in action.
A group of researchers at the University of Rhode Island, USA, tested whether Utricularia macrorhiza, the common North American bladderworth, could be an effective predator of mosquito larvae. By adding U. macrorhiza to containers with larvae of A. aegypti and A. albopictus, they were able to kill 95 to 100% of the larvae in only five days. That’s an amazing result, don’t you think?
Bladderwort with several Aedes larvae (marked with asterisks) in its traps. Credits to Couret et al. (2020).*
Since bladderworts are much easier to raise in tanks and other containers in your backyard than animal predators such as fish and dragonflies, they are a promising new alternative to control the populations of this disease-carrying insects.
So, are you eager to raise some aquatic carnivorous plants to help fight these heinous mosquitoes?
So we are going through a kind of apocalypse as everyone knows. An aggressive and contagious virus has spread all over the world and is causing a major impact in our society, killing thousands of people and crashing the economy.
But I’m not here to talk about how to protect against the virus and who is more vulnerable to it. You can find such information virtually everywhere (but don’t trust the bullshit that Karen the anti-vaxxer or your uncle Donald the boomer is spreading through Whatsapp. That is worse than the virus). Likewise, I will not point out how this pandemic is a direct outcome of our flawed capitalist society and how the fucking rich should be beheaded once and for all. No. I will make a more biological approach and explain a little bit of what this virus is from a structural, functional and taxonomic point of view.
So let’s start with what is a virus.
A virus is basically a parasitic piece of sh… genetic material that infects cells in order to reproduce. Viruses are not quite living beings as they neither have cells nor metabolism. However, they need cells to reproduce. All viruses consists of a strand of nucleic acid (either DNA or RNA) and a capsid, a “box” that protects the nucleic acid. The capsid is usually formed by many copies of one or two proteins that are encoded in the virus’ genetic material. Each individual protein molecule of the capsid is called a capsomere.
Scheme of a helical virus showing the helical capsid in green and the genetic material in blue. Credits to Anderson Brito.*
The Tobacco mosaic virus, that infects tobacco plants and others, has a typical helical capsid.
Most viruses have either a helical or an icosahedral capsid. In a helical capsid, the capsomeres are helically arranged and form an elongate and hollow tube inside of which the genetical material is located. In icosahedral capsids, the capsomeres are arranged to form a icosahedron, i.e., a polyhedron with 20 faces that surrounds the genetic material.
Scheme of an icosahedral virus with an icosahedral capsid (green) surrounding the genetic material (red). Credits to Anderson Brito.*
Adenoviruses are an example of virus with icosahedral capsids. Photo by Graham Beards.**
Many viruses have an additional coat, the envelope, that surrounds the capsid. The envelope is a bi-lipid layer crossed by glycoproteins, like the cell membrane of living organisms, and is formed by the cell membrane or an internal membrane of the cell in which the virus was born. It is, therefore, very similar to the cell membrane of the virus’ host.
Scheme of an enveloped icosahedral virus. The bi-lipid layer is shown in gray and the glycoproteins in orange. Credits to Anderson Brito.*
Zika virus (digitally colored blue in this electron microphotograph) is an envoloped icosahedral virus.
Regarding the type of nucleic acid found in viruses, they can be classified into three main groups: DNA viruses, RNA viruses and retroviruses.
DNA viruses have DNA as their nucleic acid. When they infect a cell, they are delivered into the cell’s nucleus, where they depend entirely on the cell’s machinery to reproduce, i.e., they use the hosts DNA-polymerase to produce new DNA strands and the host’s RNA-polymerase to build a viral RNA that will, in turn, be converted into the capsid proteins using the cell’s ribosomes. DNA viruses suffer little mutation because DNA-polymerase enzymes have a proofreading ability, i.e., they can detect errors during replication and fix them. Viruses such as Herpesvirus (which cause herpes and chicken pox), Poxvirus (which include the now extinct Variola virus that caused smallpox) and Adenovirus are all DNA viruses.
The Human alphaherpesvirus 3 (HHV-3) is an enveloped icosahedral DNA virus that causes chickenpox and shingles in humans.
RNA viruses, also called riboviruses, on the other hand, have RNA as their nucleic acid. When they infect a cell, they usually remain in the cell’s cytoplasm. Different from DNA viruses, RNA viruses often have their own RNA-polymerase enzyme and use it to produce new copies but still depend on the host’s ribosomes to translate their RNA into proteins to build the capsid and make new copies of their RNA polymerase. Since RNA-polymerase enzymes lack the proofreading ability of DNA-polymerase, RNA viruses mutate rapidly. A lot of human diseases are caused by RNA viruses, incluing the common cold, influenza, ebola, yellow fever, dengue fever, Zika fever, hepatitis C, rabies, polio, measles, as well as COVID-19, caused by the current apocalypse-driving coronavirus.
The Yellow fever virus is an enveloped icosahedral RNA virus.
Retroviruses, the last virus type, also have RNA as their nucleic acid. However, different from RNA viruses, retroviruses do not produce new copies directly from their RNA using a RNA-polymerase. Instead of that, they have another type of enzyme, called reverse transcriptase, that builds a DNA strain from their RNA. This viral DNA is then incorporated into the DNA of the host cell by an integrase enzyme. Retroviruses, therefore, change the host’s genome, i.e., they create a “hybrid” of themselves and the host. The infected cell then transcribes the viral DNA back into RNA, making several copies that allow to virus to reproduce. The most famous retroviruses to infect humans are Human immunodeficiency virus (HIV) and Hepatitis B virus.
Human Imunodeficiency Virus 1 is an enveloped icosahedral retrovirus that causes AIDS in humans.
But now let’s focus on our current celebrity, SARS-CoV-2, colloquially known as the coronavirus. This virus, which is causing the current apocalypse, is a new strain, discovered in late 2019, of the Severe acute respiratory syndrome-related coronavirus (SARSr-CoV). The previous SARS outbreak between 2002-2004 was caused by another strain of this same species, SARS-CoV, or now often referred to as SARS-CoV-1. This virus belongs to the genus Betacoronavirus and the family Coronaviridae. All members of the family Coronaviridae are often called “coronavirus” and the currently known species infect birds and mammals.
SARS-CoV-2 with artificial colors showing the “corona” (in orange) formed by the club-shaped glycoproteins of its envelope.
Coronaviruses are RNA-viruses, as mentioned above, and have a helical capsid, as well as an envelope. This envelope contains large club-shaped proteins that appear as projections on the virus surface and, in electron micrographs, resemble the solar corona, hence the name coronavirus. The envelope is built from the membrane of the host’s endoplasmic reticulum but includes glycoproteins of viral origin, including the club-shaped glycoproteins that characterize these viruses.
The presence of this envelope around the capsid has some advantages and some disadvantages to coronaviruses and any other enveloped virus. Since this envelope is basically a piece of the host’s cell, enveloped viruses can sneak into new hosts more easily because the immune system takes some time to recognize them as invaders since they are wearing a host’s “clothing”. On the other hand, this envelope is very fragile when exposed to the outer environment and degrades very quickly, so that the virus needs close contact of an infect host with a new host in order to spread. This is also why washing your hands with soap kills the virus so easily. If the virus were not enveloped, i.e., had only its capsid, it would be much more resistant.
The club-like glycoproteins of the viral envelope are also the responsible for the virus ability to infect. These glycoproteins connect to the angiotensin-converting enzyme 2 (ACE2), an enzyme that is found on the surface of many human cells. ACE2 is especially abundant in the lungs, which is the reason why this is the organ that suffers the most during SARS-CoV infections.
The main genera inside the family Coronaviridae are Alphacoronavirus, Betacoronavirus, Gammacoronavirus and Deltacoronavirus. Most known species of Alpha- and Betacoronavirus infect bats, so it is likely that the ancestor of these genera was originally a bat-specific virus that later mutated and acquired the ability to infect other species. All coronaviruses that infect humans belong to this two genera and include, besides SARS-CoV, MERS-CoV (which causes the Midle East Respiratory Syndrome) and several viruses that cause mild cold-like symptoms, such as HCoV-HKU1, HCoV-NL63 and HCoV-229E. Species of Gammacoronavirus infect mainly birds, although at least one species, Coronavirus HKU15, causes diarrhea in pigs. The genus Deltacoronavirus includes the Avian coronavirus (IBV), which causes infectious bronchitis in birds, and the Beluga whale coronavirus SW1, the only coronavirus known to infect a marine mammal.
Avian coronavirus. The club-shaped glycoproteins are clearly visible on the envelopes.
The genome of coronaviruses has about 30 thousand nucleotides, being some of the largest genomes among RNA viruses. The only known RNA virus with a larger genome, with about 41 thousand nucleotides, was discovered in 2018 and infects, guess what, planarians! Named Planarian secretory cell nidovirus (PSCNV), it belongs to the order Nidovirales, which includes coronaviruses and many other RNA-viruses, but seems to have diverged from most members of Nidovirales a long long time ago. Maybe I’ll talk more about this particular virus and the implications of its discovery in a future post.
Let’s conclude this post with a quick review of what we have learned about SARS-CoV-2, the “coronavirus”:
It is an RNA-virus, meaning that it has a great mutation potential and is able to create copies of itself in the host’s cytoplasm, being an almost self-suficient virus;
It has a helical capsid surrounding its RNA;
It has an envelope derived from the membrane of the host’s endoplasmic reticulum, which is the reason why it can be so easily killed by water and soap;
This envelope includes large clube-like glycoproteins that make it appear as a solar corona in electron micrographs, hence the name coronavirus;
It is a member of the genus Betacoronavirus, which includes a lot of species known to infect bats and that’s the reason why its origin in a Chinese bat soup is very likely.
I hope that this post helped you see more about this new virus than its ability to collapse human societies.
I recently presented a thrips in the Friday Fellow section, in that case a thrips that infects mostly fig trees. This group of insects, which make up the insect order Thysanoptera, is poorly known by the general public, but is certainly known by gardeners and farmers, as they can be a serious nuisance for many plant types.
We could imagine thrips as being kind of the mosquitoes of plants. They pierce the surface of plants and suck their juices just like mosquitoes do with vertebrates. And we all know that a mosquito bite may lead to much more than a small blood loss and local irritation of the skin. Many parasites use mosquitoes as vectors to travel from host to host, including protists such as Plasmodium falciparum, which causes malaria, and many types of virus, such as those of the genus Flavivirus, which cause the yellow, dengue and zika fevers.
A similar thing happens in the association of thrips with plants. A special genus of virus, called Tospovirus, infects many plant species and uses thrips as a vector. Inside the thrips bodies, the viruses reproduce after infecting the epithelial cells of the gut and, from there, travel via blood to the salivary glands and, when a thrips perforates a plant, the virus is injected in it. The cycle is basically the same used by Flavivirus in mosquitoes and ticks to infect vertebrates. Isn’t it amazing how a virus such as Tospovirus can infect both an animal and a plant? But what exactly is the disease caused by these viruses?
Basil leaf infected with the tomato spotted wilt virus. Photo by Scot Nelson.**
One of the most common Tospovirus is the so-called Tomato spotted wilt virus (TSWV), which is considered one of the most economically devastating plant viruses in the world. It can infect many crops, such as tomato, tobacco, bellpepper, peanut and basil. The symptoms vary from plant to plant, but usually include stunting, poorly developed fruits, commonly with ring spots on the surface, and necrosis of the leaves. It is transmitted to plants by thrips of the genus Frankliniella, mainly the western flower thrips Frankliniella occidentalis. Although the virus usually needs several hours to be able to reinfect a plant after infecting a thrips, in ideal conditions the time can e as short as five minutes.
The western flower thrips Frankliniella occidentalis. Photo by Dave Kirkeby.*
But why would a thrips feed on an obviously sick plant, all ugly and full of spots? They would certainly prefer a healthy plant, but that would prevent the virus to spread. As a result, the virus developed several strategies to attract the thrips. The TSWV is able to increase the amount of free aminoacids in infected plants, and these are essential nutrients for egg production in thrips. As a consequence, infected plants become more nutritious and attract more thrips. Feeding on infected plants, the thrips will certainly get infected and at the same time ingest more nutrients than non-infected thrips. Thus, a sick thrips actually has an increased fitness and usually lays more eggs. The plants would certainly get effing scared if they were able to have emotions.
The Soybean vein necrosis virus (SVNV) is another Tospovirus of economic concern. As it names suggests, it attacks mainly soy plants, and its main vector is the soybean thrips Neohydatothrips variabilis. Infected soybean thrips produce significantly more offspring than non-infected ones, although heavily infected individuals lay few viable eggs. How do thrips bypass this problem? It’s simple! Once they are infected, they stop feeding on infected plants and prefer non-infected ones, which increases their reproductive success by avoiding becoming heavily infected and at the same time they spread the virus further to non-infected plants. A nightmare for the plants once more.
Soybean thrips Hydatothrips variabilis. Photo by Even Dankowicz.***
A recent study investigated the relationship of another Tospovirus-thrips pair, this time of the iris yellow spot virus (IYSV), which commonly attacks garlic and onion plants, and its main vector, the onion thrips, Thrips tabaci. Infected thrips did not show an increased daily fecundity but had an increased lifespan, allowing them to lay more eggs simply because they lived longer.
But the effect of Tospovirus on thrips can go further. For example, although plants infected by the TSWV release more aminoacids that attract and increase the fecundity of thrips, the infections still seems to have some deleterious effects on the insect. Infected males of Frankliniella occidentalis increase their consumption of food juices and increase the transmission of the virus. Females, on the other hand, seem to need nutrients that cannot be found in plants. As a result, they increase the consumption of eggs of the two-spotted spider mite Tetranychus urticae, with which they often coexist. Although primarily herbivorous as most thrips, the western flower thrips eventually feeds on mite eggs, and being infected by TSWV makes females become more eager to eat eggs. This is certainly not a strategy of the virus itself as the other ones, since a female that is feeding on mite eggs does not contribute for the virus’ reproductive success. Nevertheless, this is an interesting phenomenon that show us how the interactions in a trophic web can be dynamic, changing, for example, due to an uninentional side effect of a virus trying to survive.
Keough S, Han J, Shuman T, Wise K, Nachappa P (2016) Effects of Soybean Vein Necrosis Virus on Life History and Host Preference of Its Vector, Neohydatothrips variabilis , and Evaluation of Vector Status of Frankliniella tritici and Frankliniella fusca. Journal of Economic Entomology 109(5): 1979–1987. doi: 10.1093/jee/tow145
Leach A, Fuchs M, Harding R, Nault BA (2019) Iris Yellow Spot Virus Prolongs the Adult Lifespan of Its Primary Vector, Onion Thrips (Thrips tabaci) (Thysanoptera: Thripidae). Journal of Insect Science 19(3): 8. doi: 10.1093/jisesa/iez041
Shrestha A, Srinivasan R, Riley DG, Culbreath AK (2012) Direct and indirect effects of a thrips‐transmitted Tospovirus on the preference and fitness of its vector, Frankliniella fusca. Entomologia Experimentalis et Applicata 145(3): 260–271. doi: 10.1111/eea.12011
Stafford-Banks CA, Yang LH, McMunn MS, Ullman DE (2014) Virus infection alters the predatory behavior of an omnivorous vector. Oikos 123(11): 1384–1390. doi: 10.1111/oik.01148
About a year ago, almost nobody on the whole world was aware of the existence of a virus named Zika virus and the illness it may cause in humans, the Zika fever or Zika disease. But is this a new, previously unknown virus? Where did it come from and why is it suddenly of so much concern?
The Zika virus, or ZIKV, is a virus in the genus Flavivirus, which also include other viruses, such as the ones responsible for the dengue fever and the yellow fever. The name Flavivirus means “yellow virus” in Latin, due to the yellow fever. All the three diseases are transmitted to humans throughs mosquitoes, especially the widespread Aedes aegypti.
The mosquito Aedes aegypti is currently the main vector of the Zika virus. Photo by James Gathany.
The Zika virus was discovered in 1947 in Uganda in a febrile rhesus monkey in the Zika Forest, hence the name. From 1951 on, serological studies indicated that the virus could also infect humans, as antibodies against the virus were found in the blood of humans in several African and Asian countries, such as Central African Republic, Egypt, Gabon, Sierra Leone, Tanzania, Uganda, India, Indonesia, Malaysia, the Philippines, Thailand and Vietnam.
In 1968, in Nigeria, the virus was isolated from humans for the first time. During the following decades of the 20th century, the virus was detected via serological evidence or isolated directly in many humans. However, despite the confirmation of this virus in humans, research developed very slowly, most likely because the affected countries don’t have enough resources to conduct the necessary studies and richer countries are not at all interested in the health of the poor ones.
There was a small increase in concern over the virus after it was detected outside Africa and Asia for the first time, in 2007, in the Yap Island, Micronesia. After that, some epidemics occurred in several archipelagoes in the Pacific.
Since last year, the Zika virus has been dectected in South America and started to spread rapidly across the countries. It was suggested that the virus reached Brazil in 2014 during the World Cup. (Thanks, FIFA!). By November 2015, the disease has reached Mexico, which means it is about to reach the United States! Now suddenly it started to be of a major concern worlwide.
Currently known distribution of the Zika virus in humans. Map of the United States Centers for Disease Control and Prevention.
Common symptoms of the Zika fever include mild headaches, fever, joint pains and rash. It was not considered a serious disease, as it usually fades quickly after a week, until recently, when it was linked to the development of microcephaly in fetuses of mothers infected by the virus during the first trimester of pregnancy.
I wonder how many children were born with microcephaly in Africa and Asia during the last decades because there was no investment to study the virus. Now that it suddenly became a worldwide threat, there is no vaccine, no adequate treatment and most physicians are unable to identify the illness through the symptoms.
And there are a lot of other viruses forgotten in poor tropical countries just waiting for the right opportunity to spread and scare North America and Europe. No one cares while they remain among poor African and Asian people, but global warming is here and tropical diseases love it more than anything else.
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References:
Gatherer, D. & Kohl, A., (2015). Zika virus: a previously slow pandemic spreads rapidly through the Americas Journal of General Virology DOI: 10.1099/jgv.0.000381
Hayes, E. B. 2009. Zika Virus Outside Africa. Emerging Infectious Diseases, 15(9): 1347-1350.
Vasconcelos, P. (2015). Doença pelo vírus Zika: um novo problema emergente nas Américas? Revista Pan-Amazônica de Saúde, 6 (2), 9-10 DOI: 10.5123/S2176-62232015000200001
This work is licensed under a Creative Commons Attribution 4.0 International License.
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