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I know it is an unconventional way to describe viruses, but would it still be technically correct?
In genetics, genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations
While some viruses tend to cause mutations, most don't have such a strong mutagenesis effect. As such, they are not really genotoxic. Also, even if a virus is genotoxic, one should definitely not reduce the activity of a virus to its genotoxicity. A virus has a life-cycle and is able to reproduce. It is clearly more than a simple genotoxic chemical agent such as metal chromium.
So, in short
- Reducing viruses to their genotoxic effect would be a misrepretentation of what virsues are
- Most viruses don't have a strong genotoxic effect and therefore you can not make the claim in the general sense.
Class 8 Science Chapter 2 MCQ
Class 8 Science Chapter 2 MCQ (Multiple Choice Questions) of Microorganism: Friend and Foe. There are 25 MCQ Tests containing more than 100 questions with answers and explanation, prepared for new academic session 2021-22.
MCQ are prepared from NCERT Textbook of Class 8 Science and Exemplar book including all the best questions for practice.
Class 8 Science Chapter 2 MCQ for 2021-22
Class 8 Science Chapter 2 MCQ Tests for Exams
Class 8 Science Chapter 2 MCQ Tests of Microorganism: Friend and Foe with complete explanation and answers. All the questions have four option with one option correct. After attempting you can see the answer and explanation for justification. All the important topics of NCERT Books 8th Science Chapter 2 have been added in these MCQs.
Preservatives, prevent the spoilage of foods leaves for a long time from microbial infection. We used in kitchen:
Preservatives (vinegar, common salt, oil) prevent the spoilage of foods leaves for a long time from microbial infection.
Which of the following reproduces only inside a host cell?
Virus is a micro-organism, which is in an inactive or dead from outside the body of a host. It reproduces or replicates only when it enters a host and reaches its cells.
Paheli is writing some sentences about “algae”. In which of sentences, she is writing as incorrect?
Spirogyra is multi-celled algae. Chlamydomonas and diatoms are single-celled algae. Blue-green algae can fix nitrogen gas of atmosphere.
In which of the following statement is or are incorrect?
Here, all the options are correct. Hence, your answer will be option [D].
Paheli wants to write some correct statements. Would you help her?
Here, all the options are correct. Hence, your answer will be option [D].
In which of the following human diseases are caused by protozoa?
Female Anopheles mosquito which carries the parasite of malaria. Female Aedes mosquito acts as carrier of dengue virus. Malaria is caused by the protozoan parasite Plasmodium.
Paheli wants to know the method for preventing the occurrence or spread of communicable diseases:
Here, all the statements are correct about the preventing the occurrence or spreading of communicable diseases. Hence, your answer will be option [D].
The disease caused by a protozoan and spread by an insect is
Malaria is the disease which is caused by the spread of a “Protozoan” i.e. “Plasmodium”. It is spread in healthy individuals by the bite of a female “Anopheles Mosquito” caring this “Plasmodium” in their mouth (saliva).
Asthma is a chronic inflammatory disease in lungs. Name the fungus, who is responsible for this?
Allergic bronchopulmonary aspergillosis (ABPA) is a condition characterized by an exaggerated response of the immune system (a hypersensitivity response) to the fungus Aspergillus fumigatus.
The precaution is observed in the use of antibiotics. Choose the incorrect sentence(s):
Antibiotics should be taken only on the advice of “Qualified Doctor”. Qualified doctor means a person who is legally qualified to practice medicine doctor of medicine. In the other words, a person who engaged in general medical practice, as distinguished from one specializing in surgery.
Types of Fungi
|Moulds:||Multi cellular organisms.|
|Mushrooms:||Multi cellular organisms.|
The Common Characters of Viruses
- They are the smallest living organisms.
- They do not have a cellular structure.
- They have a simple structure, consisting of a small piece of Nucleic Acid (either DNA or RNA), surrounded by a protein coat.
- They are on the boundary between living and non-living.
Discovery of Viruses
In 1852, a Russian botanist D.I. Ivanovsky discovered viruses from tobacco plants. These viruses were named as TMV (Tabacco Mosaic Viruses). Viruses are the smallest living organisms, ranging in size from about 20-300 mm on average. They cannot be seen with the simple microscope. They pass through filters which retain bacteria.
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What is micro-biology?
There is a world of living organisms which cannot be seen with the naked eyes. They can be seen only through a microscope. Microorganisms are often described as single -celled or unicellular organisms, but there are certain species that are multi-cellulars. The study of micro-organisms is called micro-biology.
What are Extremophiles?
Micro-organisms are found in a variety of places, and they can survive in extremely harsh environmental
conditions. Some types of micro-organisms have adapted to the extreme conditions and sustained colonies these organisms are known as Extremophiles.
What is Bacteriology?
Becteria are microscopic, unicellualar organisms. They are often coocus -(Spherical) or red-shaped and 0.5- 51/m in the longest dimension. The study of bacteria is known as Bacteriology.
What are Pathogens?
Some micro-organisms are useful to us in many ways, while some are definitely harmful since they cause diseases. The microorganisms which cause disease are known as Pathogens.
What are DNA Viruses?
DNA viruses are viruses that contain DNA genomes. Some viruses contain double-stranded DNA genomes while some contain single-stranded DNA genome. Hence, they belong to group 1 and group 2 of Baltimore classification. Furthermore, this genome can be linear or segmented.
Figure 01: DNA Virus
Moreover, these viruses are usually large, icosahedral, enveloped in lipoproteins, and they do not have polymerase enzymes. Whenever they replicate, they use either host DNA polymerases or virally encoded DNA polymerases. Moreover, they cause latent infections. Some examples of DNA viruses are Herpes viruses, poxviruses, hepadnaviruses, and hepatitis B.
It’s a little more complicated
In short, yes. Or at least there’s plenty to suggest that the line between living and non-living might be a little blurry.
For one thing, some viruses do contain parts of the molecular machinery required to replicate themselves. The gigantic mimivirus – a virus so large that it was initially mistaken for a bacterium, and has a genome larger than that of some bacteria – carries genes that enable the production of amino acids and other proteins that are required for translation, the process that for viruses turns genetic code into new viruses. (Mimivirus still lacks ribosomal DNA, which codes for the assembly of proteins that carries out the translation process.)
Another sign of fuzzy boundaries between living and non-living is that viruses share a lot of their genetics with their host cells. A 2015 study of protein folds, structures that change little during evolution, in thousands of organisms and viruses, found 442 folds shared across all and only 66 that were specific to viruses.
These findings suggest that viruses may have evolved alongside the very first ‘living’ cells. As Gustavo Caetano-Anollés, one of the authors of the protein fold study, explains, “We need to broaden how we define life and its associated activities.”
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As viruses are obligate intracellular pathogens they cannot replicate without the machinery and metabolism of a host cell. Although the replicative life cycle of viruses differs greatly between species and category of virus, there are six basic stages that are essential for viral replication.
1. Attachment: Viral proteins on the capsid or phospholipid envelope interact with specific receptors on the host cellular surface. This specificity determines the host range (tropism) of a virus.
2. Penetration: The process of attachment to a specific receptor can induce conformational changes in viral capsid proteins, or the lipid envelope, that results in the fusion of viral and cellular membranes. Some DNA viruses can also enter the host cell through receptor-mediated endocytosis.
3. Uncoating: The viral capsid is removed and degraded by viral enzymes or host enzymes releasing the viral genomic nucleic acid.
4. Replication: After the viral genome has been uncoated, transcription or translation of the viral genome is initiated. It is this stage of viral replication that differs greatly between DNA and RNA viruses and viruses with opposite nucleic acid polarity. This process culminates in the de novo synthesis of viral proteins and genome.
5. Assembly: After de novo synthesis of viral genome and proteins, which can be post-transrciptionally modified, viral proteins are packaged with newly replicated viral genome into new virions that are ready for release from the host cell. This process can also be referred to as maturation.
6. Virion release: There are two methods of viral release: lysis or budding. Lysis results in the death of an infected host cell, these types of viruses are referred to as cytolytic. An example is variola major also known as smallpox. Enveloped viruses, such as influenza A virus, are typically released from the host cell by budding. It is this process that results in the acquisition of the viral phospholipid envelope. These types of virus do not usually kill the infected cell and are termed cytopathic viruses.
After virion release some viral proteins remain within the host’s cell membrane, which acts as potential targets for circulating antibodies. Residual viral proteins that remain within the cytoplasm of the host cell can be processed and presented at the cell surface on MHC class-I molecules, where they are recognised by T cells.
Virus replication © The copyright for this work resides with the author
Structure of Viruses
Viruses vary in their structure. A virus particle consists of DNA or RNA within a protective protein coat called a capsid. The shape of the capsid may vary from one type of virus to another. The capsid is made from the proteins that are encoded by viral genes within their genome.
The shape of the capsid serves as one basis for classification of viruses. The capsid of the virus shown in Figure below is icosahedral. Virally coded proteins will self-assemble to form a capsid. Some viruses have an envelope of phospholipids and proteins. The envelope is made from portions of the host&rsquos cell membrane. It surrounds the capsid and helps protect the virus from the host&rsquos immune system. The envelope may also have receptor molecules that can bind with host cells. They make it easier for the virus to infect the cells.
Diagram of a Cytomegalovirus. The capsid encloses the genetic material of the virus. The envelope which surrounds the capsid is typically made from portions of the host cell membranes (phospholipids and proteins). Not all viruses have a viral envelope.
Helical capsids are made up of a single type of protein subunit stacked around a central axis to form a helical structure. The helix may have a hollow center, which makes it look like a hollow tube. This arrangement results in rod-shaped or filamentous virions. These virions can be anything from short and very rigid, to long and very flexible. The well-studied tobacco mosaic virus (TMV) is an example of a helical virus, as seen in the Figure below.
A helical virus, tobacco mosaic virus. Although their diameter may be very small, some helical viruses can be quite long, as shown here. 1. Nucleic acid 2. Viral protein units, 3. Capsid. TMV causes tobacco mosaic disease in tobacco, cucumber, pepper, and tomato plants.
Icosahedral capsid symmetry gives viruses a spherical appearance at low magnification, but the protein subunits are actually arranged in a regular geometrical pattern, similar to a soccer ball they are not truly spherical. An icosahedral shape is the most efficient way of creating a hardy structure from multiple copies of a single protein. This shape is used because it can be built from a single basic unit protein which is used over and over again. This saves space in the viral genome.
Adenovirus, an icosahedral virus. An icosahedron is a three-dimensional shape made up of 20 equilateral triangles. Viral structures are built of repeated identical protein subunits, making the icosahedron the easiest shape to assemble using these subunits.
Complex viruses possess a capsid which is neither purely helical, nor purely icosahedral, and which may have extra structures such as protein tails or a complex outer wall. Viral protein subunits will self-assemble into a capsid, but the complex viruses DNA also codes for proteins which help in building the viral capsid. Many phage viruses are complex-shaped they have an icosahedral head bound to a helical tail. The tail may have a base plate with protein tail fibers. Some complex viruses do not have tail fibers.
This &ldquomoon lander&rdquo-shaped complex virus infects Escherichia coli bacteria.
Some viruses are able to surround (envelop) themselves in a portion of the cell membrane of their host. The virus can use either the outer membrane of the host cell, or an internal membrane such as the nuclear membrane or endoplasmic reticulum. In this way the virus gains an outer lipid bilayer known as a viral envelope. This membrane is studded with proteins coded for by both the viral genome and the host genome. However, the lipid membrane itself and any carbohydrates present come entirely from the host cell. The influenza virus, HIV, and the varicella zoster virus (Figure below) are enveloped viruses.
An enveloped virus. Varicella zoster virus causes chicken pox and shingles.
The viral envelope can give a virus some advantages over other capsid-only viruses. For example, they have better protection from the host's immune system, enzymes and certain chemicals. The proteins in the envelope can include glycoproteins, which act as receptor molecules. These receptor molecules allow host cells to recognize and bind the virions, which may result in easier uptake of the virion into the cell. Most enveloped viruses depend on their envelopes to infect cells. However, because the envelope contains lipids, it makes the virus more susceptible to inactivation by environmental agents, such as detergents that disrupt lipids.
WHO Deletes Naturally Acquired Immunity from Its Website
Maybe you have some sense that something fishy is going on? Same. If it’s not one thing, it’s another.
Coronavirus lived on surfaces until it didn’t. Masks didn’t work until they did, then they did not. There is asymptomatic transmission, except there isn’t. Lockdowns work to control the virus except they do not. All these people are sick without symptoms until, whoops, PCR tests are wildly inaccurate because they were never intended to be diagnostic tools. Everyone is in danger of the virus except they aren’t. It spreads in schools except it doesn’t.
On it goes. Daily. It’s no wonder that so many people have stopped believing anything that “public health authorities” say. In combination with governors and other autocrats doing their bidding, they set out to take away freedom and human rights and expected us to thank them for saving our lives. At some point this year (for me it was March 12) life began feeling like a dystopian novel of your choice.
Well, now I have another piece of evidence to add to the mile-high pile of fishy mess. The World Health Organization, for reasons unknown, has suddenly changed its definition of a core conception of immunology: herd immunity. Its discovery was one of the major achievements of 20th century science, gradually emerging in the 1920s and then becoming ever more refined throughout the 20th century.
Herd immunity is a fascinating observation that you can trace to biological reality or statistical probability theory, whichever you prefer. (It is certainly not a “strategy” so ignore any media source that describes it that way.) Herd immunity speaks directly, and with explanatory power, to the empirical observation that respiratory viruses are either widespread and mostly mild (common cold) or very severe and short-lived (SARS-CoV-1).
Why is this? The reason is that when a virus kills its host – that is, when a virus overtaxes the body’s ability to integrate it, its host dies and so the virus does not spread to others. The more this occurs, the less it spreads. If the virus doesn’t kill its host, it can hop to others through all the usual means. When you get a virus and fight it off, your immune system encodes that information in a way that builds immunity to it. When it happens to enough people (and each case is different so we can’t put a clear number on it, especially given so many cross immunities) the virus loses its pandemic quality and becomes endemic, which is to say predictable and manageable. Each new generation incorporates that information through more exposure.
This is what one would call Virology/Immunology 101. It’s what you read in every textbook. It’s been taught in 9th grade cell biology for probably 80 years. Observing the operations of this evolutionary phenomenon is pretty wonderful because it increases one’s respect for the way in which human biology has adapted to the presence of pathogens without absolutely freaking out.
And the discovery of this fascinating dynamic in cell biology is a major reason why public health became so smart in the 20th century. We kept calm. We managed viruses with medical professionals: doctor/patient relationships. We avoided the Medieval tendency to run around with hair on fire but rather used rationality and intelligence. Even the New York Times recognizes that natural immunity is powerful with Covid-19, which is not in the least bit surprising.
Until one day, this strange institution called the World Health Organization – once glorious because it was mainly responsible for the eradication of smallpox – has suddenly decided to delete everything I just wrote from cell biology basics. It has literally changed the science in a Soviet-like way. It has removed with the delete key any mention of natural immunities from its website. It has taken the additional step of actually mischaracterizing the structure and functioning of vaccines.
So that you will believe me, I will try to be as precise as possible. Here is the website from June 9, 2020. You can see it here on Archive.org. You have to move down the page and click on the question about herd immunity. You see the following.
That’s pretty darn accurate overall. Even the statement that the threshold is “not yet clear” is correct. There are cross immunities to Covid from other coronaviruses and there is T cell memory that contributes to natural immunity.
Some estimates are as low as 10%, which is a far cry from the modelled 70% estimate of virus immunity that is standard within the pharmaceutical realm. Real life is vastly more complicated than models, in economics or epidemiology. The WHO’s past statement is a solid, if “pop,” description.
However, in a screenshot dated November 13, 2020, we read the following note that somehow pretends as if human beings do not have immune systems at all but rather rely entirely on big pharma to inject things into our blood.
What this note at the World Health Organization has done is deleted what amounts to the entire million-year history of humankind in its delicate dance with pathogens. You could only gather from this that all of us are nothing but blank and unimprovable slates on which the pharmaceutical industry writes its signature.
In effect, this change at WHO ignores and even wipes out 100 years of medical advances in virology, immunology, and epidemiology. It is thoroughly unscientific – shilling for the vaccine industry in exactly the way the conspiracy theorists say that WHO has been doing since the beginning of this pandemic.
What’s even more strange is the claim that a vaccine protects people from a virus rather than exposing them to it. What’s amazing about this claim is that a vaccine works precisely by firing up the immune system through exposure. Why I had to type those words is truly beyond me. This has been known for centuries. There is simply no way for medical science completely to replace the human immune system. It can only game it via what used to be called inoculation.
Take from this what you will. It is a sign of the times. For nearly a full year, the media has been telling us that “science” requires that we comply with their dictates that run contrary to every tenet of liberalism, every expectation we’ve developed in the modern world that we can live freely and with the certainty of rights. Then “science” took over and our human rights were slammed. And now the “science” is actually deleting its own history, airbrushing over what it used to know and replacing it with something misleading at best and patently false at worst.
I cannot say why, exactly, the WHO did this. Given the events of the past nine or ten months, however, it is reasonable to assume that politics are at play. Since the beginning of the pandemic, those who have been pushing lockdowns and hysteria over the coronavirus have resisted the idea of natural herd immunity, instead insisting that we must live in lockdown until a vaccine is developed.
That is why the Great Barrington Declaration, written by three of the world’s preeminent epidemiologists and which advocated embracing the phenomenon of herd immunity as a way of protecting the vulnerable and minimizing harms to society, was met with such venom. Now we see the WHO, too, succumbing to political pressure. This is the only rational explanation for changing the definition of herd immunity that has existed for the past century.
The science has not changed only the politics have. And that is precisely why it is so dangerous and deadly to subject virus management to the forces of politics. Eventually the science too bends to the duplicitous character of the political industry.
When the existing textbooks that students use in college contradict the latest official pronouncements from the authorities during a crisis in which the ruling class is clearly attempting to seize permanent power, we’ve got a problem.
Editorial addition, January 4, 2021: WHO has changed it definition yet again, to incorporate the obvious reality of natural immunity.
No, the coronavirus wasn’t made in a lab. A genetic analysis shows it’s from nature
The SARS-CoV-2 virus (seen in this transmission electron microscope image of virus isolated from a U.S. patient), which causes COVID-19, was rumored to be human-made, but scientists have now debunked that theory.
The coronavirus pandemic circling the globe is caused by a natural virus, not one made in a lab, a new study says.
The virus’s genetic makeup reveals that SARS-CoV-2 isn’t a mishmash of known viruses, as might be expected if it were human-made. And it has unusual features that have only recently been identified in scaly anteaters called pangolins, evidence that the virus came from nature, Kristian Andersen and his colleagues report March 17 in Nature Medicine.
When Andersen, an infectious disease researcher at the Scripps Research Institute in La Jolla, Calif., first heard about the coronavirus causing an outbreak in China, he wondered where the virus came from. Initially, researchers thought the virus was being spread by repeated infections jumping from animals in a seafood market in Wuhan, China, into humans and then being passed person to person. Analysis from other researchers has since suggested that the virus probably jumped only once from an animal into a person and has been spread human to human since about mid-November (SN: 3/4/20).
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But shortly after the virus’s genetic makeup was revealed in early January, rumors began bubbling up that maybe the virus was engineered in a lab and either intentionally or accidentally released.
An unfortunate coincidence fueled conspiracy theorists, says Robert Garry, a virologist at Tulane University in New Orleans. The Wuhan Institute of Virology is “in very close proximity to” the seafood market, and has conducted research on viruses, including coronaviruses, found in bats that have potential to cause disease in people. “That led people to think that, oh, it escaped and went down the sewers, or somebody walked out of their lab and went over to the market or something,” Garry says.
Accidental releases of viruses, including SARS, have happened from other labs in the past. So “this is not something you can just dismiss out of hand,” Andersen says. “That would be foolish.”
Looking for clues
Andersen assembled a team of evolutionary biologists and virologists, including Garry, from several countries to analyze the virus for clues that it could have been human-made, or grown in and accidentally released from a lab.
“We said, ‘Let’s take this theory — of which there are multiple different versions — that the virus has a non-natural origin … as a serious potential hypothesis,’ ” Andersen says.
Meeting via Slack and other virtual portals, the researchers analyzed the virus’s genetic makeup, or RNA sequence, for clues about its origin.
It was clear “almost overnight” that the virus wasn’t human-made, Andersen says. Anyone hoping to create a virus would need to work with already known viruses and engineer them to have desired properties.
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But the SARS-CoV-2 virus has components that differ from those of previously known viruses, so they had to come from an unknown virus or viruses in nature. “Genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone,” Andersen and colleagues write in the study.
“This is not a virus somebody would have conceived of and cobbled together. It has too many distinct features, some of which are counterintuitive,” Garry says. “You wouldn’t do this if you were trying to make a more deadly virus.”
Other scientists agree. “We see absolutely no evidence that the virus has been engineered or purposely released,” says Emma Hodcroft, a molecular epidemiologist at the University of Basel in Switzerland. She was not part of Andersen’s group, but is a member of a team of scientists with Nextstrain.org that is tracking small genetic changes in the coronavirus to learn more about how it is spreading around the world.
That finding debunks a widely disputed analysis, posted at bioRxiv.org before peer review, that claimed to find bits of HIV in the coronavirus, Hodcroft says. Other scientists quickly pointed out flaws in the study and the authors retracted the report, but not before it fueled the notion that the virus was engineered.
Some stretches of the virus’s genetic material are similar to HIV, but that’s something that stems from those viruses sharing a common ancestor during evolution, Hodcroft says. “Essentially their claim was the same as me taking a copy of the Odyssey and saying, ‘Oh, this has the word the in it,’ and then opening another book, seeing the word the in it and saying, ‘Oh my gosh, it’s the same word, there must be parts of the Odyssey in this other book,” she says. “It was a really misleading claim and really bad science.”
Finding peculiar features
Andersen’s group next set out to determine whether the virus could have been accidentally released from a lab. That’s a real possibility because researchers in many places are working with coronaviruses that have potential to infect humans, he says. “Stuff comes out of the lab sometimes, almost always accidentally,” he says.
A couple of unexpected features of the virus caught the researchers’ eyes, Andersen says. In particular, the gene encoding the coronavirus’s spike protein has 12 extra RNA building blocks, or nucleotides, stuck in it.
This spike protein protrudes from the virus’ surface and allows the virus to latch onto and enter human cells. That insertion of RNA building blocks adds four amino acids to the spike protein, and creates a site in the protein for an enzyme called furin to cut. Furin is made in human cells, and cleaves proteins only at spots where a particular combination of amino acids is found, like the one created by the insertion. SARS and other SARS-like viruses don’t have those cutting sites.
See all our coverage of the coronavirus outbreak
Finding the furin cutting site was a surprise: “That was an aha moment and an uh-oh moment,” Garry says. When bird influenza viruses acquire the ability to be cut by furin, the viruses often become more easily transmissible. The insertion also created places where sugar molecules could be fastened to the spike protein, creating a shield to protect the virus from the immune system.
The COVID-19 virus’ spike protein also binds more tightly to a protein on human cells called ACE2 than SARS does (SN: 3/10/20). Tighter binding may allow SARS-CoV-2 to more easily infect cells. Together, those features may account for why COVID-19 is so contagious (SN: 3/13/20).
“It’s very peculiar, these two features,” Andersen says. “How do we explain how this came about? I’ve got to be honest. I was skeptical [that it was natural]. This could have happened in tissue culture” in a lab, where viruses may acquire mutations as they replicate many times in lab dishes. In nature, viruses carrying some of those mutations might be weeded out by natural selection but might persist in lab dishes where even feeble viruses don’t have to fight hard for survival.
Clinching the case for nature
But then the researchers compared SARS-CoV-2 with other coronaviruses recently found in nature, including in bats and pangolins. “It looks like SARS-CoV-2 could be a mix of bat and pangolin viruses,” Garry says.
Viruses, especially RNA viruses such as coronaviruses, often swap genes in nature. Finding genes related to the pangolin viruses was especially reassuring because those viruses’ genetic makeup wasn’t known until after SARS-CoV-2’s discovery, making it unlikely anyone was working with them in a lab, he says.
Coronaviruses that infect pangolins gave researchers important clues that the SARS-CoV-2 virus is natural. 2630ben/iStock/Getty Images Plus
In particular, pangolins also have the amino acids that cause the tight binding of the spike protein to ACE2, the team found. “So clearly, this is something that can happen in nature,” Andersen says. “I thought that was very important little clue. It shows there’s no mystery about its tighter binding to the human [protein] because pangolins do it, too.”
The sugar-attachment sites were another clue that the virus is natural, Andersen says. The sugars create a “mucin shield” that protects the virus from an immune system attack. But lab tissue culture dishes don’t have immune systems, making it unlikely that such an adaptation would arise from growing the virus in a lab. “That sort of explained away the tissue-culture hypothesis,” he says.
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Similarity of SARS-CoV-2 to bat and pangolin viruses is some of the best evidence that the virus is natural, Hodcroft says. “This was just another animal spillover into humans,” she says. “It’s really the most simple explanation for what we see.” Researchers still aren’t sure exactly which animal was the source.
Andersen says the analysis probably won’t lay conspiracy theories to rest. Still, he thinks the analysis was worth doing. “I was myself skeptical at the beginning and I kept flipping back and forth,” Andersen says, but he’s now convinced. “All the data show it’s natural.”
Questions or comments on this article? E-mail us at [email protected]
K. G. Andersen et al. The proximal origin of SARS-CoV-2. Nature Medicine. Published online March 17, 2020. doi: 10.1038/s41591-020-0820-9.
Genomic Instability and Aging
Genomic instability has long been considered to be a central driving force in aging, and extensive evidence has accumulated over the years supporting DNA-damage accumulation with age and its role in genomic instability. The findings that compromised genome-maintenance results in shortened life spans of model organisms or in human premature-aging syndromes suggest that genome maintenance is indeed a central antiaging mechanism.
However, aging of an organism is a very complex process, during which different tissues gradually functionally deteriorate. Since each tissue has its own characteristics and challenges, it is likely that their functional deterioration also follows individual patterns. Vijg and Dolle have put forward a model, according to which aging is not a clonal phenomenon, but rather arises from increasing heterogeneity of the cells in a tissue  . At the level of cells, accumulation of random mutations can contribute to this heterogeneity. At the level of tissues, different challenges to genomic integrity may promote aging. For instance, neural cells, which have high respiratory requirements, may be more susceptible to the accumulation of oxidative damage and cell death, whereas T cells that rely on continued proliferation may be more susceptible to senescence caused by telomere shortening.
If genomic instability is considered as a mechanism driving this age-associated mosaicism by contributing accumulation of mutations and promoting downstream outcomes such as altered gene expression, cell-cycle arrest, or cell death ( Fig. 29.2 ), a better mechanistic understanding of what triggers age-related deterioration of genome-maintenance mechanisms or changes in nuclear architecture may provide valuable insights into the role of genomic instability in aging. In addition, a better understanding of interactions between cells and tissues in the aging organism will help in determining a hierarchy of age-related changes.
Figure 29.2 . Mechanisms contributing to genomic instability and their role during aging.
Gray bubbles represent DNA lesions, arrows indicate contributions of processes to the given outcomes, and two-directional arrows indicate interplay between two processes.
Steps of the Lytic Cycle
Adsorption and Penetration
Adsorption is the process through which a bacteria gets its DNA or RNA into the host cell. This is labeled as 1 in the image above. The capsid, or protein coat around the viral genome, consists of very specific proteins. This sheild of proteins not only comes together to protect the viral genes, it serves as a sort of “key” to unlock a cell. The surface of the proteins are shaped to interact with proteins on the surface of the host cell.
During the lytic cycle, the replication of viral genes is carried out a number of times by a hijacked cellular system. Remember that the virus itself has imported few, if any, supporting proteins. Thus, the viral DNA must produce these in order to hijack the cell’s processes. The first proteins created are often created as the cell reads its own DNA and produces proteins. The viral genes simply sneak into the process. This creates what are called viral early proteins.
These early proteins have important functions (to the virus) of commandeering the cell’s machinery. They clear the cell’s normal metabolic agenda, and turn many of its activities toward the replication of viral genes and the production of viral proteins. The virus uses the raw products the cell has assembled (amino acids and nucleic acids) as building blocks for the parts it needs.
While this may seem like an overly complex process for such a small virus genome, consider first that there are really only a handful of proteins. Most viruses produce and code for only a handful of proteins. Unlike cells, a virus doesn’t need the complex proteins required to metabolize energy. As obligate parasites, a virus is dependent upon its host cell’s ability to provide raw materials. This makes it one of the most efficient forms of DNA replication that we know of.
Assembly and Release
As these parts are built, their natural evolutionary shapes help them come together in the proper way. Since most of the components are proteins, they have formed over evolutionary time to be able to come together with very little outside influence. The assembly of new virions is a hallmark of the lytic cycle. The other viral life cycle does not include producing and assembling new virions.
In this way, the lytic cycle resembles a small virus factory. All of the parts of the virus are produced independently, then assembled, and finally released into the environment. While the image above shows only 3 assembled virions at stage 6, in reality there would be millions. Compare the lytic cycle to the lysogenic cycle below it, in which an accurate 2 copies are shown after 1 bacterial division.
1. Which of the following represents the lytic cycle?
A. Viral DNA is replicated as the host cell divides.
B. The viral genome takes over the host cell, and creates a virus factory.
C. The viral genome is mostly dormant.
2. Which life cycle, the lytic cycle or the lysogenic cycle, produces the most virions?
A. It depends
B. The lytic cycle
C. The lysogenic cycle
3. Based on what you now know about the lytic cycle, why is it so hard to eradicate the common cold?
A. It shouldn’t be!
B. The virus changes too much.
C. In targeting the mechanisms viruses use, you target the mechanisms every cell uses.