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Can a virus infect a virus?

Can a virus infect a virus?


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As far as I know a virus can infect any cellular organism from a bacteria onwards, including protists, algae, plants, and so forth.

But can a virus infect a virus?


No, it cannot. Viruses infect cells, in order to use the cellular machinery to replicate themselves - viruses themselves do not possess such a machinery, so speaking of one virus infecting another is meaningless.

This does not mean that viruses do not interact: when two viruses co-infect the same cell, the progeny virions may contain parts of the genomes of both viruses. This is how genetic recombination occurs in HIV.

An even more famous example is gene reshuffling of influenza viruses, where an animal virus exchanges its genes with a human virus, producing a new human strain. In the popular culture some of these a famously named after animals whose virus contributed or animals where the reshuffling has occured (bird's flu, swine flu, etc.)

Update
It is worth mentioning the satellite viruses, which are viruses that lack the proteins necessary to catalize the replication and possibly even the genes coding for their capsid proteins (in which case they are more properly called satellite nucleic acids rather than satellite viruses). These viruses are dependent on a helper virus to carry the missing genes. This is not characterized as parasitism, but it is rather close.

Update 2
A special type of satellite viruses, called virophages, actually do exhibit characteristics of parasitism in respect to the helper virus:

Unlike satellite viruses, virophages have a parasitic effect on their co-infecting virus. Virophages have been observed to render a giant virus inactive and thereby improve the condition of the host organism.

Flu Season Looms And Scientists Wonder How Flu And COVID-19 Might Mix

This negative-stained transmission electron micrograph depicts the ultrastructural details of an influenza virus particle, or virion.

With the annual flu season about to start, it's still unclear exactly how influenza virus will interact with the coronavirus if a person has both viruses.

Doctors around the world have seen some patients who tested positive for both influenza virus and the coronavirus that causes COVID-19. At least a couple of dozen cases have been reported — although that's not a lot, given that over 26 million people have tested positive for SARS-CoV-2, the virus that causes COVID-19.

Still, "it is quite possible and likely that the two viruses could infect a patient at the same time or, for that matter, sequentially: one month, one virus, and the next month, the other virus," says Michael Matthay, a professor of medicine at the University of California, San Francisco.

Both viruses can cause dangerous inflammation in the lungs that can fill the airspaces with fluid, making it difficult to breathe, he notes.

"It's likely with both viruses at the same time, the severity of respiratory failure would be greater," says Matthay. "Or, of course, having two illnesses in a row that affected the lungs would make the respiratory failure more severe."

COVID-19 is so new, though, that scientists just don't have enough research to know for sure.

Generally speaking, co-infections are common when it comes to respiratory diseases. Helen Chu, an associate professor of medicine at the University of Washington in Seattle, has done studies to screen people with respiratory symptoms for a variety of viruses.

"We often find the presence of more than one virus at a time," says Chu, but that doesn't necessarily mean that there's actually more than one active infection. "You could be at the end of your illness, so you are no longer symptomatic from it, but you can still detect nonviable virus."

Goats and Soda

From Southern Hemisphere, Hints That U.S. May Be Spared Flu On Top Of COVID-19

One study looked at people who tested positive for SARS-CoV-2 and found that about 20% tested positive for at least one other respiratory virus, such as rhinovirus — which is a common cold virus — or respiratory syncytial virus (RSV), which can be serious in infants and older adults.

Past research suggests that viruses can have complicated interactions when two are present. An extra virus can do nothing at all, can make an illness more severe or possibly even have some kind of short-term protective effect.

For example, it's unclear if rhinovirus can make a bout with flu worse, says Chu.

"But for a lot of the other viruses that are known causes of disease like parainfluenza virus and human metapneumovirus and human coronavirus, those can work with flu and cause you to have more severe disease," says Chu.

Not everyone agrees on that. "There are many studies all over the map," says Sarah Meskill, assistant professor of pediatrics and emergency medicine at Baylor College of Medicine in Houston.

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"The studies looking at previous coronavirus infection with influenza are so sparse it's really hard to know," adds Meskill, saying that her gut reaction is that "we're going to see co-infections, we are going to see patients positive for both" flu virus and the coronavirus.

Some epidemiological research shows that respiratory viruses can compete with each other in a way that means one virus can suppress the spread of another.

RSV and influenza virus are a good example of that, says Meskill, explaining that when both try to infect the same cell, one will win. What's more, when RSV levels in a population tend to be high, levels of flu tend to be low, and vice versa.

Tanya Miura, a virologist at the University of Idaho, says that when a new pandemic flu virus swept through in 2009, "it was delayed in certain populations that were having ongoing outbreaks of other respiratory viruses at the time."

Her work with lab animals shows that getting a mild respiratory virus can seem to offer some protection against getting a different, more severe one a couple of days later.

In the Southern Hemisphere, where the flu season is just coming to an end, doctors saw very little flu at all this year, probably mostly because of travel restrictions, the wearing of masks and social distancing.

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And the number of circulating respiratory viruses does seem to be lower up north, too, says Chu, who has been searching for them in her city: "There's really no transmission of these other viruses going on in the community right now. That is what we are seeing in Seattle."

The flu isn't completely absent, though. "I can tell you that we're starting to find flu," says Chu. "It's very important to get vaccinated."

Getting vaccinated against seasonal flu would both protect people against a double whammy from the flu and COVID-19 and reduce the total number of flu cases. That would help a health care system that is struggling to cope with one serious respiratory illness already.

It's worth noting that the symptoms of the flu — fever, muscle aches, cough — can be very similar to those of COVID-19.

"Just because you test positive for the flu doesn't mean you don't have coronavirus," says Meskill. "You should still be doing your social distancing and quarantining."

And some researchers are getting ready to look at people who have mostly recovered from the flu and then get COVID-19. "Is it going to make it worse? Is it going to limit the virus or the transmission?" wonders Stacey Schultz-Cherry, an infectious diseases researcher at St. Jude Children's Research Hospital in Memphis, Tenn. "We're actually starting those studies soon."


Understanding How Giant Viruses Can Infect Cells

Melting permafrost has been revealing some remarkably well-preserved and extremely old stuff, like a prehistoric puppy and giant viruses. Researchers are trying to learn more about these giant viruses, which are changing what we know about microbes. The typical cold virus is about 30 nanometers in size, while giant viruses are over 300 nanometers. A critical question is whether they can infect cells, and new work reported in Cell suggests they can. While it's still unclear whether the ones we've found could get into human cells and what would happen once they got there, researchers are trying to learn more about the conditions that enable these viruses to enter a cell and cause infection.

"Giant viruses are gargantuan in size and complexity," said the principal study investigator Kristin Parent, associate professor of Biochemistry and Molecular Biology at Michigan State University (MSU). "The giant viruses recently discovered in Siberia retained the ability to infect after 30,000 years in permafrost."

Scientists at MSU have been able to develop a model for investigating giant viruses, which can clearly withstand very harsh conditions. The viral genomes in this study are encased in a structure called a capsid that often contains viral genomes, in the case of the six viruses studied in this work, it is an icosahedral-shaped capsid. The researchers looked at the structures the viruses could form during different stages of infection, which was challenging.

"Giant viruses are difficult to image due to their size and previous studies relied on finding the 'one-in-a-million' virus in the correct state of infection," Parent said.

The team had to subject the viruses to various treatments to mimic what they might encounter while trying to infect a cell, and used cryo-electron microscopy and scanning electron microscopy to visualize the viruses under different conditions. "Cryo-EM allows us to study viruses and protein structures at the atomic level and to capture them in action," Parent said.

The viruses use a process that applies a starfish-shaped seal and a portal called stargate to release its genome into a host cell. Low pH, high salt, and high temperature all induced the stargate opening, and each condition triggered a different stage of infection.

"We discovered that the starfish seal above the stargate portal slowly unzips while remaining attached to the capsid rather than simply releasing all at once," Parent explained. "Our description of a new giant virus genome release strategy signifies another paradigm shift in our understanding of virology. This new model now allows scientists to mimic the stages reliably and with high frequency, opening the door for future study and dramatically simplifying any studies aimed at the virus."

Researchers can also now learn more about the proteins encoded by viral genes. "The results of this study help to assign putative&mdashor assumed&mdashroles to many proteins with previously unknown functions, highlighting the power of this new model," Parent said. "We identified key proteins released during the initial stages of infection responsible for helping mediate the process and complete the viral takeover." There is still a lot more work to be done, unsurprisingly.

"The exact functions of many of these proteins and how they orchestrate giant virus infection are prime candidates for future study," Parent added. "Many of the proteins we identified matched proteins that one would expect to be released during the initial stages of viral infections. This greatly supports our hypothesis that the in vitro stages generated in this study are reflective of those that occur in vivo."

Virologists are still debating and investigating whether giant viruses can infect people.


Coronavirus outbreak raises question: Why are bat viruses so deadly?

It’s no coincidence that some of the worst viral disease outbreaks in recent years — SARS, MERS, Ebola, Marburg and likely the newly arrived 2019-nCoV virus — originated in bats.

A new University of California, Berkeley, study finds that bats’ fierce immune response to viruses could drive viruses to replicate faster, so that when they jump to mammals with average immune systems, such as humans, the viruses wreak deadly havoc.

Some bats — including those known to be the original source of human infections — have been shown to host immune systems that are perpetually primed to mount defenses against viruses. Viral infection in these bats leads to a swift response that walls the virus out of cells. While this may protect the bats from getting infected with high viral loads, it encourages these viruses to reproduce more quickly within a host before a defense can be mounted.

This makes bats a unique reservoir of rapidly reproducing and highly transmissible viruses. While the bats can tolerate viruses like these, when these bat viruses then move into animals that lack a fast-response immune system, the viruses quickly overwhelm their new hosts, leading to high fatality rates.

“Some bats are able to mount this robust antiviral response, but also balance it with an anti-inflammation response,” said Cara Brook, a postdoctoral Miller Fellow at UC Berkeley and the first author of the study. “Our immune system would generate widespread inflammation if attempting this same antiviral strategy. But bats appear uniquely suited to avoiding the threat of immunopathology.”

The researchers note that disrupting bat habitat appears to stress the animals and makes them shed even more virus in their saliva, urine and feces that can infect other animals.

“Heightened environmental threats to bats may add to the threat of zoonosis,” said Brook, who also works with a Madagascar-based field project that explores the link between loss of bat habitat and the spillover of bat viruses into other animals and humans.

“The bottom line is that bats are potentially special when it comes to hosting viruses,” said Mike Boots, a disease ecologist and UC Berkeley professor of integrative biology. “It is not random that a lot of these viruses are coming from bats. Bats are not even that closely related to us, so we would not expect them to host many human viruses. But this work demonstrates how bat immune systems could drive the virulence that overcomes this.”

The new study by Brook, Boots and their colleagues was published this month in the journal eLife.

Boots and UC Berkeley colleague Wayne Getz are among 23 Chinese and American co-authors of a paper published last week in the journal EcoHealth that argues for better collaboration between U.S. and Chinese scientists who are focused on disease ecology and emerging infections.

Vigorous flight leads to longer lifespan – and perhaps viral tolerance

As the only flying mammal, bats elevate their metabolic rates in flight to a level that doubles that achieved by similarly sized rodents when running.

The Egyptian fruit bat, Rousettus aegyptiacus, is a host to the Marburg virus, which can infect monkeys and cross over into humans to cause a deadly hemorrhagic fever (Photo courtesy of Victor Corman)

Generally, vigorous physical activity and high metabolic rates lead to higher tissue damage due to an accumulation of reactive molecules, primarily free radicals. But to enable flight, bats seem to have developed physiological mechanisms to efficiently mop up these destructive molecules.

This has the side benefit of efficiently mopping up damaging molecules produced by inflammation of any cause, which may explain bats’ uniquely long lifespans. Smaller animals with faster heart rates and metabolism typically have shorter lifespans than larger animals with slower heartbeats and slower metabolism, presumably because high metabolism leads to more destructive free radicals. But bats are unique in having far longer lifespans than other mammals of the same size: Some bats can live 40 years, whereas a rodent of the same size may live two years.

This rapid tamping down of inflammation may also have another perk: tamping down inflammation related to antiviral immune response. One key trick of many bats’ immune systems is the hair-trigger release of a signaling molecule called interferon-alpha, which tells other cells to “man the battle stations” before a virus invades.

Brook was curious how bats’ rapid immune response affects the evolution of the viruses they host, so she conducted experiments on cultured cells from two bats and, as a control, one monkey. One bat, the Egyptian fruit bat (Rousettus aegyptiacus), a natural host of Marburg virus, requires a direct viral attack before transcribing its interferon-alpha gene to flood the body with interferon. This technique is slightly slower than that of the Australian black flying fox (Pteropus alecto), a reservoir of Hendra virus, which is primed to fight virus infections with interferon-alpha RNA that is transcribed and ready to turn into protein. The African green monkey (Vero) cell line does not produce interferon at all.

As shown in this model of viral infection (click to view animated GIF), when green monkey (Vero) cells are invaded by a virus, they quickly succumb because they have no interferon response. Susceptible cells (green pixels) are rapidly exposed, infected and killed (purple). (UC Berkeley images by Cara Brook)

When challenged by viruses mimicking Ebola and Marburg, the different responses of these cell lines were striking. While the green monkey cell line was rapidly overwhelmed and killed by the viruses, a subset of the rousette bat cells successfully walled themselves off from viral infection, thanks to interferon early warning.

In the Australian black flying fox cells, the immune response was even more successful, with the viral infection slowed substantially over that in the rousette cell line. In addition, these bat interferon responses seemed to allow the infections to last longer.

“Think of viruses on a cell monolayer like a fire burning through a forest. Some of the communities — cells — have emergency blankets, and the fire washes through without harming them, but at the end of the day you still have smoldering coals in the system — there are still some viral cells,” Brook said. The surviving communities of cells can reproduce, providing new targets for the the virus and setting up a smoldering infection that persists across the bat’s lifespan.

Brook and Boots created a simple model of the bats’ immune systems to recreate their experiments in a computer.

In a model of viral infection (click to view animated GIF), when cells of the Australian black flying fox are invaded by a virus, some quickly wall themselves off from infection, having been forewarned by a rapid release of interferon from dying cells. This allows the cells to survive longer, but increases the number of infectious cells (red). (UC Berkeley images by Cara Brook)

“This suggests that having a really robust interferon system would help these viruses persist within the host,” Brook said. “When you have a higher immune response, you get these cells that are protected from infection, so the virus can actually ramp up its replication rate without causing damage to its host. But when it spills over into something like a human, we don’t have those same sorts of antiviral mechanism, and we could experience a lot of pathology.”

The researchers noted that many of the bat viruses jump to humans through an animal intermediary. SARS got to humans through the Asian palm civet MERS via camels Ebola via gorillas and chimpanzees Nipah via pigs Hendra via horses and Marburg through African green monkeys. Nonetheless, these viruses still remain extremely virulent and deadly upon making the final jump into humans.

Brook and Boots are designing a more formal model of disease evolution within bats in order to better understand virus spillover into other animals and humans.

“It is really important to understand the trajectory of an infection in order to be able to predict emergence and spread and transmission,” Brook said.

Other co-authors of the eLife paper are Kartik Chandran and Melinda Ng of Albert Einstein College of Medicine in New York City Andrew Dobson, Andrea Graham, Bryan Grenfell and Anieke van Leeuwen of Princeton University in New Jersey Christian Drosten and Marcel Müller of Humboldt University in Berlin, Germany and Lin-Fa Wang of Duke University-National University of Singapore Medical School.

The work was funded by a National Science Foundation fellowship, the Miller Institute for Basic Research at UC Berkeley and a grant from the National Institutes of Health (R01 AI134824).


Viruses

Viruses are tiny infectious agents that invade host cells and cause disease. Although they are harmful, viruses also have interesting technological potential.

Virus

Viruses are microscopic biological agents that invade living hosts and infect their bodies by reproducing within their cell tissue.

Photograph by Maryna Olyak

Viruses are tiny infectious agents that rely on living cells to multiply. They may use an animal, plant, or bacteria host to survive and reproduce. As such, there is some debate as to whether or not viruses should be considered living organisms. A virus that is outside of a host cell is known as a virion.

Not only are viruses microscopic, they are smaller than many other microbes, such as bacteria. Most viruses are only 20&ndash400 nanometers in diameter, whereas human egg cells, for example, are about 120 micrometers in diameter, and the E. coli bacteria has a diameter of around 1 micrometer. Viruses are so small that they are best viewed using an electron microscope, which is how they were first visualized in the 1940s.

Viruses generally come in two forms: rods or spheres. However, bacteriophages (viruses that infect bacteria) have a unique shape, with a geometric head and filamentous tail fibers. No matter the shape, all viruses consist of genetic material (DNA or RNA) and have an outer protein shell, known as a capsid.

There are two processes used by viruses to replicate: the lytic cycle and lysogenic cycle. Some viruses reproduce using both methods, while others only use the lytic cycle. In the lytic cycle, the virus attaches to the host cell and injects its DNA. Using the host&rsquos cellular metabolism, the viral DNA begins to replicate and form proteins. Then fully formed viruses assemble. These viruses break, or lyse, the cell and spread to other cells to continue the cycle.

Like the lytic cycle, in the lysogenic cycle the virus attaches to the host cell and injects its DNA. From there, the viral DNA gets incorporated into the host&rsquos DNA and the host&rsquos cells. Each time the host&rsquos cells go through replication, the virus&rsquos DNA gets replicated as well, spreading its genetic information throughout the host without having to lyse the infected cells.

In humans, viruses can cause many diseases. For example, the flu is caused by the influenza virus. Typically, viruses cause an immune response in the host, and this kills the virus. However, some viruses are not successfully treated by the immune system, such as human immunodeficiency virus, or HIV. This leads to a more chronic infection that is difficult or impossible to cure often only the symptoms can be treated.

Unlike bacterial infections, antibiotics are ineffective at treating viral infections. Viral infections are best prevented by vaccines, though antiviral drugs can treat some viral infections. Most antiviral drugs work by interfering with viral replication. Some of these drugs stop DNA synthesis, preventing the virus from replicating

Although viruses can have devastating health consequences, they also have important technological applications. Viruses are particularly vital to gene therapy. Because some viruses incorporate their DNA into host DNA, they can be genetically modified to carry genes that would benefit the host. Some viruses can even be engineered to reproduce in cancer cells and trigger the immune system to kill those harmful cells. Although this is still an emerging field of research, it gives viruses the potential to one day do more good than harm.

Viruses are microscopic biological agents that invade living hosts and infect their bodies by reproducing within their cell tissue.


Understanding How Giant Viruses Can Infect Cells

Melting permafrost has been revealing some remarkably well-preserved and extremely old stuff, like a prehistoric puppy and giant viruses. Researchers are trying to learn more about these giant viruses, which are changing what we know about microbes. The typical cold virus is about 30 nanometers in size, while giant viruses are over 300 nanometers. A critical question is whether they can infect cells, and new work reported in Cell suggests they can. While it's still unclear whether the ones we've found could get into human cells and what would happen once they got there, researchers are trying to learn more about the conditions that enable these viruses to enter a cell and cause infection.

"Giant viruses are gargantuan in size and complexity," said the principal study investigator Kristin Parent, associate professor of Biochemistry and Molecular Biology at Michigan State University (MSU). "The giant viruses recently discovered in Siberia retained the ability to infect after 30,000 years in permafrost."

Scientists at MSU have been able to develop a model for investigating giant viruses, which can clearly withstand very harsh conditions. The viral genomes in this study are encased in a structure called a capsid that often contains viral genomes, in the case of the six viruses studied in this work, it is an icosahedral-shaped capsid. The researchers looked at the structures the viruses could form during different stages of infection, which was challenging.

"Giant viruses are difficult to image due to their size and previous studies relied on finding the 'one-in-a-million' virus in the correct state of infection," Parent said.

The team had to subject the viruses to various treatments to mimic what they might encounter while trying to infect a cell, and used cryo-electron microscopy and scanning electron microscopy to visualize the viruses under different conditions. "Cryo-EM allows us to study viruses and protein structures at the atomic level and to capture them in action," Parent said.

The viruses use a process that applies a starfish-shaped seal and a portal called stargate to release its genome into a host cell. Low pH, high salt, and high temperature all induced the stargate opening, and each condition triggered a different stage of infection.

"We discovered that the starfish seal above the stargate portal slowly unzips while remaining attached to the capsid rather than simply releasing all at once," Parent explained. "Our description of a new giant virus genome release strategy signifies another paradigm shift in our understanding of virology. This new model now allows scientists to mimic the stages reliably and with high frequency, opening the door for future study and dramatically simplifying any studies aimed at the virus."

Researchers can also now learn more about the proteins encoded by viral genes. "The results of this study help to assign putative&mdashor assumed&mdashroles to many proteins with previously unknown functions, highlighting the power of this new model," Parent said. "We identified key proteins released during the initial stages of infection responsible for helping mediate the process and complete the viral takeover." There is still a lot more work to be done, unsurprisingly.

"The exact functions of many of these proteins and how they orchestrate giant virus infection are prime candidates for future study," Parent added. "Many of the proteins we identified matched proteins that one would expect to be released during the initial stages of viral infections. This greatly supports our hypothesis that the in vitro stages generated in this study are reflective of those that occur in vivo."

Virologists are still debating and investigating whether giant viruses can infect people.


Biology 171

By the end of this section, you will be able to do the following:

  • Identify major viral illnesses that affect humans
  • Compare vaccinations and anti-viral drugs as medical approaches to viruses

Viruses cause a variety of diseases in animals, including humans, ranging from the common cold to potentially fatal illnesses like meningitis ((Figure)). These diseases can be treated by antiviral drugs or by vaccines however, some viruses, such as HIV, are capable both of avoiding the immune response and of mutating within the host organism to become resistant to antiviral drugs.


Vaccines for Prevention

The primary method of controlling viral disease is by vaccination , which is intended to prevent outbreaks by building immunity to a virus or virus family ((Figure)). Vaccines may be prepared using live viruses, killed viruses, or molecular subunits of the virus. Note that the killed viral vaccines and subunit viruses are both incapable of causing disease, nor is there any valid evidence that vaccinations contribute to autism.

Live viral vaccines are designed in the laboratory to cause few symptoms in recipients while giving them protective immunity against future infections. Polio was one disease that represented a milestone in the use of vaccines. Mass immunization campaigns in the 1950s (killed vaccine) and 1960s (live vaccine) significantly reduced the incidence of the disease, which caused muscle paralysis in children and generated a great amount of fear in the general population when regional epidemics occurred. The success of the polio vaccine paved the way for the routine dispensation of childhood vaccines against measles, mumps, rubella, chickenpox, and other diseases.

The issue with using live vaccines (which are usually more effective than killed vaccines), is the low but significant danger that these viruses will revert to their disease-causing form by back mutations . Live vaccines are usually made by attenuating (weakening) the “wild-type” (disease-causing) virus by growing it in the laboratory in tissues or at temperatures different from what the virus is accustomed to in the host. Adaptations to these new cells or temperatures induce mutations in the genomes of the virus, allowing it to grow better in the laboratory while inhibiting its ability to cause disease when reintroduced into conditions found in the host. These attenuated viruses thus still cause infection, but they do not grow very well, allowing the immune response to develop in time to prevent major disease. Back mutations occur when the vaccine undergoes mutations in the host such that it readapts to the host and can again cause disease, which can then be spread to other humans in an epidemic. This type of scenario happened as recently as 2007 in Nigeria where mutations in a polio vaccine led to an epidemic of polio in that country.

Some vaccines are in continuous development because certain viruses, such as influenza and HIV, have a high mutation rate compared to that of other viruses and normal host cells. With influenza, mutations in the surface molecules of the virus help the organism evade the protective immunity that may have been obtained in a previous influenza season, making it necessary for individuals to get vaccinated every year. Other viruses, such as those that cause the childhood diseases measles, mumps, and rubella, mutate so infrequently that the same vaccine is used year after year.


Watch this NOVA video to learn how microbiologists are attempting to replicate the deadly 1918 Spanish influenza virus so they can understand more about virology.

Vaccines and Antiviral Drugs for Treatment

In some cases, vaccines can be used to treat an active viral infection. The concept behind this is that by giving the vaccine, immunity is boosted without adding more disease-causing virus. In the case of rabies, a fatal neurological disease transmitted via the saliva of rabies virus-infected animals, the progression of the disease from the time of the animal bite to the time it enters the central nervous system may be two weeks or longer. This is enough time to vaccinate individuals who suspect that they have been bitten by a rabid animal, and their boosted immune response is sufficient to prevent the virus from entering nervous tissue. Thus, the potentially fatal neurological consequences of the disease are averted, and the individual only has to recover from the infected bite. This approach is also being used for the treatment of Ebola, one of the fastest and most deadly viruses on Earth. Transmitted by bats and great apes, this disease can cause death in 70 to 90 percent of infected humans within two weeks. Using newly developed vaccines that boost the immune response in this way, there is hope that affected individuals will be better able to control the virus, potentially saving a greater percentage of infected persons from a rapid and very painful death.

Another way of treating viral infections is the use of antiviral drugs. Because viruses use the resources of the host cell for replication and the production of new virus proteins, it is difficult to block their activities without damaging the host. However, we do have some effective antiviral drugs, such as those used to treat HIV and influenza. Some antiviral drugs are specific for a particular virus and others have been used to control and reduce symptoms for a wide variety of viral diseases. For most viruses, these drugs can inhibit the virus by blocking the actions of one or more of its proteins. It is important to note that the targeted proteins be encoded by viral genes and that these molecules are not present in a healthy host cell. In this way, viral growth is inhibited without damaging the host.

Antivirals have been developed to treat genital herpes (herpes simplex II) and influenza. For genital herpes, drugs such as acyclovir can reduce the number and duration of episodes of active viral disease, during which patients develop viral lesions in their skin cells. As the virus remains latent in nervous tissue of the body for life, this drug is not curative but can make the symptoms of the disease more manageable. For influenza, drugs like Tamiflu (oseltamivir) ((Figure)) can reduce the duration of “flu” symptoms by one or two days, but the drug does not prevent symptoms entirely. Tamiflu works by inhibiting an enzyme (viral neuraminidase) that allows new virions to leave their infected cells. Thus, Tamiflu inhibits the spread of virus from infected to uninfected cells. Other antiviral drugs, such as Ribavirin, have been used to treat a variety of viral infections, although its mechanism of action against certain viruses remains unclear.


By far, the most successful use of antivirals has been in the treatment of the retrovirus HIV, which causes a disease that, if untreated, is usually fatal within 10 to 12 years after infection. Anti-HIV drugs have been able to control viral replication to the point that individuals receiving these drugs survive for a significantly longer time than the untreated.

Anti-HIV drugs inhibit viral replication at many different phases of the HIV replicative cycle ((Figure)). Drugs have been developed that inhibit the fusion of the HIV viral envelope with the plasma membrane of the host cell (fusion inhibitors), the conversion of its RNA genome into double-stranded DNA (reverse transcriptase inhibitors, like AZT), the integration of the viral DNA into the host genome (integrase inhibitors), and the processing of viral proteins (protease inhibitors).


Unfortunately, when any of these drugs are used individually, the high mutation rate of the virus allows it to easily and rapidly develop resistance to the drug, limiting the drug’s effectiveness. The breakthrough in the treatment of HIV was the development of HAART, highly active anti-retroviral therapy, which involves a mixture of different drugs, sometimes called a drug “cocktail.” By attacking the virus at different stages of its replicative cycle, it is much more difficult for the virus to develop resistance to multiple drugs at the same time. Still, even with the use of combination HAART therapy, there is concern that, over time, the virus will develop resistance to this therapy. Thus, new anti-HIV drugs are constantly being developed with the hope of continuing the battle against this highly fatal virus.

The study of viruses has led to the development of a variety of new ways to treat non-viral diseases. Viruses have been used in gene therapy . Gene therapy is used to treat genetic diseases such as severe combined immunodeficiency (SCID), a heritable, recessive disease in which children are born with severely compromised immune systems. One common type of SCID is due to the lack of an enzyme, adenosine deaminase (ADA), which breaks down purine bases. To treat this disease by gene therapy, bone marrow cells are taken from a SCID patient and the ADA gene is inserted. This is where viruses come in, and their use relies on their ability to penetrate living cells and bring genes in with them. Viruses such as adenovirus, an upper-respiratory human virus, are modified by the addition of the ADA gene, and the virus then transports this gene into the cell. The modified cells, now capable of making ADA, are then given back to the patients in the hope of curing them. Gene therapy using viruses as carriers of genes (viral vectors), although still experimental, holds promise for the treatment of many genetic diseases. Still, many technological problems need to be solved for this approach to be a viable method for treating genetic disease.

Another medical use for viruses relies on their specificity and ability to kill the cells they infect. Oncolytic viruses are engineered in the laboratory specifically to attack and kill cancer cells. A genetically modified adenovirus known as H101 has been used since 2005 in clinical trials in China to treat head and neck cancers. The results have been promising, with a greater short-term response rate to the combination of chemotherapy and viral therapy than to chemotherapy treatment alone. This ongoing research may herald the beginning of a new age of cancer therapy, where viruses are engineered to find and specifically kill cancer cells, regardless of where in the body they may have spread.

A third use of viruses in medicine relies on their specificity and involves using bacteriophages in the treatment of bacterial infections. Bacterial diseases have been treated with antibiotics since the 1940s. However, over time, many bacteria have evolved resistance to antibiotics. A good example is methicillin-resistant Staphylococcus aureus (MRSA, pronounced “mersa”), an infection commonly acquired in hospitals. This bacterium is resistant to a variety of antibiotics, making it difficult to treat. The use of bacteriophages specific for such bacteria would bypass their resistance to antibiotics and specifically kill them. Although phage therapy is in use in the Republic of Georgia to treat antibiotic-resistant bacteria, its use to treat human diseases has not been approved in most countries. However, the safety of the treatment was confirmed in the United States when the U.S. Food and Drug Administration approved spraying meats with bacteriophages to destroy the food pathogen Listeria. As more and more antibiotic-resistant strains of bacteria evolve, the use of bacteriophages might be a potential solution to the problem, and the development of phage therapy is of much interest to researchers worldwide.

Section Summary

Viruses cause a variety of diseases in humans. Many of these diseases can be prevented by the use of viral vaccines, which stimulate protective immunity against the virus without causing major disease. Viral vaccines may also be used in active viral infections, boosting the ability of the immune system to control or destroy the virus. A series of antiviral drugs that target enzymes and other protein products of viral genes have been developed and used with mixed success. Combinations of anti-HIV drugs have been used to effectively control the virus, extending the lifespans of infected individuals. Viruses have many uses in medicines, such as in the treatment of genetic disorders, cancer, and bacterial infections.

Free Response

Why is immunization after being bitten by a rabid animal so effective and why aren’t people vaccinated for rabies like dogs and cats are?

Rabies vaccine works after a bite because it takes a week for the virus to travel from the site of the bite to the central nervous system, where the most severe symptoms of the disease occur. Adults are not routinely vaccinated for rabies for two reasons: first, because the routine vaccination of domestic animals makes it unlikely that humans will contract rabies from an animal bite second, if one is bitten by a wild animal or a domestic animal that one cannot confirm has been immunized, there is still time to give the vaccine and avoid the often fatal consequences of the disease.

The vaccine Gardasil that targets human papilloma virus (HPV), the etiological agent of genital warts, was developed after the anti-HPV medication podofilox. Why would doctors still want a vaccine created after anti-viral medications were available?

Anti-viral medications treat HPV after the skin of the genitals has been infected. Conversely, Gardasil stimulates the immune system to prevent infection of the tissue, even if a person is exposed to HPV. Since HPV is often asymptomatic, particularly in men, the vaccine also controls the spread of disease (patients will not seek treatment for a disease if they do not realize they are infected).

Glossary


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GK Questions and Answers on Types of Viruses (Biology)

Viruses can infect animals, plants, fungi, and bacteria. The virus sometimes can cause a disease that may be fatal. Some virus may also have one effect on one type of organism, but a different effect on another. Viruses cannot replicate without a host so they are classified as parasitic.

1. Which of the following diseases are caused due to a virus?
A. Ebola
B. AIDS
C. SARS
D. All the above
Ans. D
Explanation: Viral diseases are diseases that are caused due to virus namely AIDS, Ebola, Influenza, SARS (Severe Acute Respiratory Syndrome), Chikungunya, Small Pox, etc.

2. Name the virus that is transmitted through the biting of infected animals, birds, and insects to a human?
A. Rabies Virus
B. Ebola Virus
C. Flavivirus
D. All the above
Ans. D
Explanation: Transmission of the virus through the biting of infected animals, birds, and insects to humans is known as Zoonoses. Examples: Rabies virus. Alphavirus, Flavivirus, Ebola virus, etc.

3. Based on host range, viruses are classified into:
A. Bacteriophage
B. Insect virus
C. Stem Virus
D. Both A and B
Ans. D
Explanation: There are four different types of viruses based on the type of host namely Animal viruses, Plant viruses, Bacteriophage and Insect virus.

4. In the host cell, replication of RNA virus took place in.
A. Nucleus
B. Cytoplasm
C. Mitochondria
D. Centriole
Ans. B
Explanation: An example of the replication of the virus within the cytoplasm in the host cell is all RNA virus except the influenza virus.

5. Which of the following statement is correct about viruses?
A. Viruses do not contain a ribosome.
B. Viruses can make protein.
C. Viruses can be categorised by their shapes.
D. Both A and C are correct
Ans. D
Explanation: Viruses do not contain ribosomes, so they cannot make proteins. That is why they are dependent on their host. Viruses have different shapes, sizes and can be categorised by their shapes.

6. Name the virus that covers himself with a modified section of the cell membrane and create a protective lipid envelope?
A. Influenza virus
B. HIV
C. Neither A nor B
D. Both A and B
Ans. D
Explanation: Some viruses cover themselves with a modified section of the cell membrane by creating a protective lipid envelope example the influenza virus and HIV.

7. A virus can spread through:
A. Contaminated food or water
B. Touch
C. Coughing
D. All the above
Ans. D
Explanation: Viruses can spread through touch, exchanges of saliva, coughing or sneezing, contaminated food or water and also through insects that carry them from one person to another.

8. After which period virus replicates in the body and starts to affect the host?
A. Incubation period
B. Uncoating
C. Penetration
D. None of the above
Ans. A
Explanation: Virus replicates in the body and starts to affect the host after a period known as the incubation period and symptoms may start to show.

9. Double-stranded DNA is found in which viruses?
A. Poxviruses
B. Poliomyelitis
C. Influenza viruses
D. None of the above
Ans. A
Explanation: Double-stranded DNA is found in poxviruses, the bacteriophages T2, T4, T6, T3, T7, Lamda, herpes viruses, adenoviruses, etc.

10. A virus is made up of a DNA or RNA genome inside a protein shell known as:
A. Capsid
B. Host
C. Envelope
D. Zombies
Ans. A
Explanation: A virus that is made up of a DNA or RNA genome inside a protein shell is known as a capsid. Some viruses have an external membrane envelope.

These are a few questions related to viruses, types, structure, classification, etc.


Wake up, herpesvirus!

Herpes simplex virus infections are common, with more than 80 percent of the world's people infected with herpes simplex virus (HSV). The virus often remains in a dormant mode in the body, which is beneficial to people who are infected because the virus doesn't cause symptoms while dormant. However, it's also harder for the immune system to find and eliminate the virus while it is dormant.

In October 2017, researchers reported in the journal PLOS Pathogens that they had figured out how to induce the virus to enter its dormant mode, and had also found the key proteins that are involved in waking it up. The findings may have implications for treating or preventing herpes infections, the researchers said. The results could point towards ways to target certain viral proteins to prevent viruses from waking up, thus preventing symptoms and the spreading of the virus to other people, or could lead to ways to get the virus to remain "awake," so that the immune system could eliminate it, the researchers said.



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