Homosexual Obsessive Compulsive Disorder (HOCD) is marked by excessive fear of becoming or being homosexual. The subjects often experience intrusive, unwanted mental images of homosexual behaviour. The excessive uncontrolled thoughts/doubts are very distressing and lead to compulsions in form of checking.
The approach to homosexual OCD will always depend on the particular needs of each patient. In more serious cases, itwill be necessary to combine the pharmacological approach ( fluoxetine ) with the psychotherapeutic. Thus, the most common and effective approach in these cases is the following:
Exposure prevention and response technique . This strategy starts from cognitive-behavioral therapy. It consists of deliberately exposing the person to those ideas that he himself feeds and that intensify his anxiety. The intention is to make you rationalize each idea, image and sensation by reducing the emotional and cognitive component to make it healthier, more integrated. This strategy is the most suitable for impulse control, obsessions, addictions, etc.
To conclude, point out that it is important to receive specialized help in this type of situation based on obsessive compulsive thoughts and behaviors. They are conditions that completely alter the functionality of the person and that, in addition, tend to intensify over time until they lead to more problems, more psychological comorbidities.
Are my emotional failures due to the fact that I am actually homosexual? These types of thoughts, when they become recurrent and limiting, define a very specific type of disorder.
Homosexual OCD defines a situation in which a person experiences constant doubts about their sexual orientation . That insecurity and that persistent doubt becomes an obsession capable of altering the relational, personal and work environment.
The mind is filled with intrusive ideas and images that further fuel doubt, to the point of leading to compulsive behaviors to alleviate that anxiety.
This condition, as peculiar as it may seem, can occur in more cases than we think. It begins between the ages of 18 and 20 and can completely condition the life of those who suffer from it . He does this to the extreme, for example, of avoiding certain situations such as going to the gym or feeling excessive discomfort with people of the same sex at work.
Now, let's clarify. This condition refers to those men and women who, being heterosexual, suddenly fear being homosexual. However, this does not demonstrate any homophobic behavior. We speak of a psychological condition defined by an irrational fear, there are therefore no variables referring to social prejudices .
Michigan State University and Stanford University scientists have invented a nanoparticle that eats away—from the inside out—portions of plaques that cause heart attacks.
Atherosclerosis is a cardiac-based disease where plaque builds up inside the body’s arteries, the blood vessels responsible for carrying oxygen-rich blood to the heart and other organs of the body. Plaque is made up of white immune blood cells, known as macrophages, fat, cholesterol, calcium, and other substances found in the blood. As this plaque hardens it narrows the arteries, limiting the flow of oxygen-rich blood around the body. This, in turn, can lead to serious problems, including heart attack, stroke, or even death.
The team states their nanoparticle reduces and stabilizes plaque, providing a potential treatment for atherosclerosis, a leading cause of death in the United States. The study is published in the journal Nature Nanotechnology.
Macrophages are a type of white blood cell in our immune system, which engulf and digest cellular debris, foreign substances, microbes, cancer cells, and anything else that does not have the type of proteins specific to healthy body cells.
Once inside the macrophages of arterial plaques, the nanoparticle delivers a drug agent that can stimulate the cell to engulf and eat cellular debris, removing the diseased/dead cells. By reinvigorating the macrophages, plaque size is reduced.
Future clinical trials on the nanoparticle are expected to reduce the risk of most types of heart attacks, with minimal side effects due to the unprecedented selectivity of the nanodrug, according to Smith. His research is focused on intercepting the signaling of the receptors in macrophages and sending a message via small molecules using Nano-immunotherapeutic platforms. Previous studies have acted on the surface of the cells, but this new approach works intracellularly and has been effective in stimulating macrophages.
"We found we could stimulate the macrophages to selectively eat dead and dying cells – these inflammatory cells are precursor cells to atherosclerosis – that are part of the cause of heart attacks," Smith said. "We could deliver a small molecule inside the macrophages to tell them to begin eating again."
This approach also has applications beyond atherosclerosis, he added.
"We were able to marry a groundbreaking finding in atherosclerosis by our collaborators with the state-of-the-art selectivity and delivery capabilities of our advanced nanomaterial platform," explained Smith. "We demonstrated the nanomaterials were able to selectively seek out and deliver a message to the very cells needed. It gives a particular energy to our future work, which will include clinical translation of these nanomaterials using large animal models and human tissue tests. We believe it is better than previous methods."
Smith has filed a provisional patent and will begin marketing it later this year.
When germs enter your body, your immune system springs into action. Here's how it works:
Bacteria and viruses like the one that causes COVID-19 have proteins called antigens on their surfaces. Each type of germ has its own unique antigen.
White blood cells of your immune system make proteins called antibodies to fight the antigen. Antibodies attach to antigens the way a key fits into a lock, and they destroy the invading germ.
Once you've been exposed to a virus, your body makes memory cells. If you're exposed to that same virus again, these cells recognize it. They tell your immune system to make antibodies against it.
Vaccines work in much the same way. They expose your body to an antigen that trains your immune system to fight that germ in the future. Because vaccines contain weakened or killed versions of viruses, you become immune without getting sick.
Why is herd immunity important?
Herd immunity occurs when a large portion of a community
(the herd) becomes immune to a disease, making the spread of disease from
person to person unlikely. As a result, the whole community becomes protected —
not just those who are immune.
Often, a percentage of the population must be capable of getting
a disease in order for it to spread. This is called a threshold proportion. If
the proportion of the population that is immune to the disease is greater than
this threshold, the spread of the disease will decline. This is known as the
herd immunity threshold.
What percentage of a community needs to be immune in order
to achieve herd immunity? It varies from disease to disease. The more
contagious a disease is, the greater the proportion of the population that
needs to be immune to the disease to stop its spread. For example, the measles
is a highly contagious illness. It's estimated that 94% of the population must
be immune to interrupt the chain of transmission.
How is herd immunity achieved?
There are two paths to herd immunity for COVID-19 — vaccines
and infection.
Vaccines
A vaccine for the virus that causes COVID-19 would be an
ideal approach to achieving herd immunity. Vaccines create immunity without
causing illness or resulting complications. Herd immunity makes it possible to
protect the population from a disease, including those who can't be vaccinated,
such as newborns or those who have compromised immune systems. Using the
concept of herd immunity, vaccines have successfully controlled deadly
contagious diseases such as smallpox, polio, diphtheria, rubella and many
others.
Reaching herd immunity through vaccination sometimes has
drawbacks, though. Protection from some vaccines can wane over time, requiring
revaccination. Sometimes people don't get all of the shots that they need to be
completely protected from a disease.
In addition, some people may object to vaccines because of
religious objections, fears about the possible risks or skepticism about the
benefits. People who object to vaccines often live in the same neighborhoods or
attend the same religious services or schools. If the proportion of vaccinated
people in a community falls below the herd immunity threshold, exposure to a
contagious disease could result in the disease quickly spreading. Measles has
recently resurged in several parts of the world with relatively low vaccination
rates, including the United States. Opposition to vaccines can pose a real
challenge to herd immunity.
Natural infection
Herd immunity can also be reached when a sufficient number
of people in the population have recovered from a disease and have developed
antibodies against future infection. For example, those who survived the 1918
flu (influenza) pandemic were later immune to infection with the H1N1 flu, a
subtype of influenza A. During the 2009-10 flu season, H1N1 caused the respiratory
infection in humans that was commonly referred to as swine flu.
However, there are some major problems with relying on
community infection to create herd immunity to the virus that causes COVID-19.
First, it isn't yet clear if infection with the COVID-19 virus makes a person
immune to future infection.
Research suggests that after infection with some
coronaviruses, reinfection with the same virus — though usually mild and only
happening in a fraction of people — is possible after a period of months or years.
Further research is needed to determine the protective effect of antibodies to
the virus in those who have been infected.
Even if infection with the COVID-19 virus creates
long-lasting immunity, a large number of people would have to become infected
to reach the herd immunity threshold. Experts estimate that in the U.S., 70% of
the population — more than 200 million people — would have to recover from
COVID-19 to halt the epidemic. If many people become sick with COVID-19 at
once, the health care system could quickly become overwhelmed. This amount of
infection could also lead to serious complications and millions of deaths,
especially among older people and those who have chronic conditions.
How can you slow the transmission of COVID-19?
Until a COVID-19 vaccine is developed, it's crucial to slow
the spread of the COVID-19 virus and protect individuals at increased risk of
severe illness, including older adults and people of any age with underlying
health conditions. To reduce the risk of infection:
Avoid large events and mass gatherings.
Avoid close contact (within about 6 feet, or 2 meters) with
anyone who is sick or has symptoms.
Stay home as much as possible and keep distance between
yourself and others (within about 6 feet, or 2 meters) if COVID-19 is spreading
in your community, especially if you have a higher risk of serious illness.
Keep in mind some people may have the COVID-19 virus and spread it to others,
even if they don't have symptoms or don't know they have COVID-19.
Wash your hands often with soap and water for at least 20
seconds, or use an alcohol-based hand sanitizer that contains at least 60%
alcohol.
Wear a cloth face covering in public spaces, such as the
grocery store, where it's difficult to avoid close contact with others, especially
if you're in an area with ongoing community spread. Only use nonmedical cloth
masks — surgical masks and N95 respirators should be reserved for health care
providers.
Cover your mouth and nose with your elbow or a tissue when
you cough or sneeze. Throw away the used tissue.
Avoid touching your eyes, nose and mouth.
Avoid sharing dishes, glasses, bedding and other household
items if you're sick.
Clean and disinfect high-touch surfaces, such as doorknobs,
light switches, electronics and counters, daily.
Stay home from work, school and public areas if you're sick,
unless you're going to get medical care. Avoid public transportation, taxis and
ride-sharing if you're sick.
Herd immunity happens when a large part of the population -- the herd -- is immune to a virus. This can happen either because these people got vaccinated or had already been infected. Herd immunity makes it harder for a virus to spread. So even those who haven't been sick or vaccinated have some protection.
The more contagious a virus is, the more people need to be immune for herd immunity to kick in. The SARS-CoV-2 virus is so contagious that experts estimate about 70% of people in a community will need to be immune to have herd protection. That number might be hard to get to without a vaccine or a whole lot of people getting sick.
If You've Had COVID-19, Are You Immune?
Health experts don't know whether we really become immune to COVID-19 after we're infected. And if we do have immunity, we don't know how long it might last. Thus far, there have been only a few incidents of confirmed re-infections. With two cases, it appears the patients were re-infected by the same strain, while the third was infected with a slightly different strain of the virus.
The disease emergence model above provides a construct for how pathogens emerge from animals and illustrates the continuum of animal pathogen infectivity in the human population. However, relatively little is known about the factors that mediate transition from one stage to the next as a pathogen of animal origin scales the stages of this paradigm Figure1, ever increasing its ability to reside in the human population and be transmitted throughout it. What is known, however, is that the interface between humans and animals is of paramount importance in the process. As we increase our interactions with animals through hunting, the trading of animal foods, animal husbandry practices, wet markets, and the domestication of animals or exotic pets, the probability of cross-species transmission dramatically increases.
Zoonotic disease emergence model outlining the 5 stages of pathogen emergence from animals to humans.
Information Theory is one of the few scientific fields fortunate enough to have an identifiable beginning - Claude Shannon's 1948 paper. The story of the evolution of how it progressed from a single theoretical paper to a broad field that has redefined our world is a fascinating one. It provides the opportunity to study the social, political, and technological interactions that have helped guide its development and define its trajectory, and gives us insight into how a new field evolves.
We often hear Claude Shannon called the father of the Digital Age. In the beginning of his paper Shannon acknowledges the work done before him, by such pioneers as Harry Nyquist and RVL. Hartley at Bell Labs in the 1920s. Though their influence was profound, the work of those early pioneers was limited and focussed on their own particular applications. It was Shannon’s unifying vision that revolutionized communication, and spawned a multitude of communication research that we now define as the field of Information Theory. One of those key concepts was his definition of the limit for channel capacity. Similar to Moore’s Law, the Shannon limit can be considered a self-fulfilling prophecy. It is a benchmark that tells people what can be done, and what remains to be done – compelling them to achieve it.
"What made possible, what induced the development of coding as a theory, and the development of very complicated codes, was Shannon's Theorem: he told you that it could be done, so people tried to do it. [Interview with Fano, R. 2001]
Quantum information science is a young field, its
underpinnings still being laid by a large number of researchers [see
"Rules for a Complex Quantum World," by Michael A. Nielsen;
Scientific American, November 2002]. Classical information science, by contrast,
sprang forth about 50 years ago, from the work of one remarkable man: Claude E.
Shannon. In a landmark paper written at Bell Labs in 1948, Shannon defined in
mathematical terms what information is and how it can be transmitted in the
face of noise. What had been viewed as quite distinct modes of
communication--the telegraph, telephone, radio and television--were unified in
a single framework.
Shannon was born in 1916 in Petoskey, Michigan, the son of a
judge and a teacher. Among other inventive endeavors, as a youth he built a
telegraph from his house to a friend's out of fencing wire. He graduated from
the University of Michigan with degrees in electrical engineering and
mathematics in 1936 and went to M.I.T., where he worked under computer pioneer
Vannevar Bush on an analog computer called the differential analyzer.
Shannon's M.I.T. master's thesis in electrical engineering
has been called the most important of the 20th century: in it the 22-year-old
Shannon showed how the logical algebra of 19th-century mathematician George
Boole could be implemented using electronic circuits of relays and switches.
This most fundamental feature of digital computers' design--the representation
of "true" and "false" and "0" and "1"
as open or closed switches, and the use of electronic logic gates to make
decisions and to carry out arithmetic--can be traced back to the insights in
Shannon's thesis.
In 1941, with a Ph.D. in mathematics under his belt, Shannon
went to Bell Labs, where he worked on war-related matters, including
cryptography. Unknown to those around him, he was also working on the theory
behind information and communications. In 1948 this work emerged in a
celebrated paper published in two parts in Bell Labs's research journal.
Quantifying Information
Shannon defined the quantity of information produced by a
source--for example, the quantity in a message--by a formula similar to the
equation that defines thermodynamic entropy in physics. In its most basic
terms, Shannon's informational entropy is the number of binary digits required
to encode a message. Today that sounds like a simple, even obvious way to
define how much information is in a message. In 1948, at the very dawn of the
information age, this digitizing of information of any sort was a revolutionary
step. His paper may have been the first to use the word "bit," short
for binary digit.
As well as defining information, Shannon analyzed the
ability to send information through a communications channel. He found that a
channel had a certain maximum transmission rate that could not be exceeded.
Today we call that the bandwidth of the channel. Shannon demonstrated
mathematically that even in a noisy channel with a low bandwidth, essentially
perfect, error-free communication could be achieved by keeping the transmission
rate within the channel's bandwidth and by using error-correcting schemes: the
transmission of additional bits that would enable the data to be extracted from
the noise-ridden signal.
Today everything from modems to music CDs rely on
error-correction to function. A major accomplishment of quantum-information
scientists has been the development of techniques to correct errors introduced
in quantum information and to determine just how much can be done with a noisy
quantum communications channel or with entangled quantum bits (qubits) whose
entanglement has been partially degraded by noise.
The Unbreakable Code
A year after he founded and launched information theory,
Shannon published a paper that proved that unbreakable cryptography was
possible. (He did this work in 1945, but at that time it was classified.) The
scheme is called the one-time pad or the Vernam cypher, after Gilbert Vernam,
who had invented it near the end of World War I. The idea is to encode the
message with a random series of digits--the key--so that the encoded message is
itself completely random. The catch is that one needs a random key that is as
long as the message to be encoded and one must never use any of the keys twice.
Shannon's contribution was to prove rigorously that this code was unbreakable.
To this day, no other encryption scheme is known to be unbreakable.
The problem with the one-time pad (so-called because an
agent would carry around his copy of a key on a pad and destroy each page of
digits after they were used) is that the two parties to the communication must
each have a copy of the key, and the key must be kept secret from spies or
eavesdroppers. Quantum cryptography solves that problem. More properly called
quantum key distribution, the technique uses quantum mechanics and entanglement
to generate a random key that is identical at each end of the quantum
communications channel. The quantum physics ensures that no one can eavesdrop
and learn anything about the key: any surreptitious measurements would disturb
subtle correlations that can be checked, similar to error-correction checks of
data transmitted on a noisy communications line.
Encryption based on the Vernam cypher and quantum key
distribution is perfectly secure: quantum physics guarantees security of the
key and Shannon's theorem proves that the encryption method is unbreakable.
[For Scientific American articles on quantum cryptography and other
developments of quantum information science during the past decades, please
click here.]
A Unique, Unicycling Genius
Shannon fit the stereotype of the eccentric genius to a T.
At Bell Labs (and later M.I.T., where he returned in 1958 until his retirement
in 1978) he was known for riding in the halls on a unicycle, sometimes juggling
as well [see "Profile: Claude E. Shannon," by John Horgan; Scientific
American, January 1990]. At other times he hopped along the hallways on a pogo
stick. He was always a lover of gadgets and among other things built a robotic
mouse that solved mazes and a computer called the Throbac ("THrifty
ROman-numeral BAckward-looking Computer") that computed in roman numerals.
In 1950 he wrote an article for Scientific American on the principles of
programming computers to play chess [see "A Chess-Playing Machine,"
by Claude E. Shannon; Scientific American, February 1950].
In the 1990s, in one of life's tragic ironies, Shannon came
down with Alzheimer's disease, which could be described as the insidious loss
of information in the brain. The communications channel to one's
memories--one's past and one's very personality--is progressively degraded
until every effort at error correction is overwhelmed and no meaningful signal
can pass through. The bandwidth falls to zero. The extraordinary pattern of
information processing that was Claude Shannon finally succumbed to the
depredations of thermodynamic entropy in February 2001. But some of the signal
generated by Shannon lives on, expressed in the information technology in which
our own lives are now immersed.
Both bacteria and viruses are so small that they can only be seen through a microscope, and both have the ability to cause infection, but that’s where the similarities end.
Bacteria
Bacteria are one-celled organisms that can be found naturally throughout our bodies and in our environment. Most are harmless and do not cause infection. Bacteria in our bodies help us to digest food, protect us against other bacteria or microbes, and provide nutrients for our body. Seen under a microscope they look like rods, balls, or spirals, and they can multiply quickly under the right conditions. Less than one per cent of bacteria actually make us sick. Infections caused by bacteria include strep throat, tuberculosis, and urinary tract infections (UTI).
Antibiotics are available to treat most bacterial infections; however, it is often best to let your body’s own immune system fight them if it is able to.
Viruses
Viruses on the other hand, cannot live without a host, or another living creature to help them multiply. Viruses are smaller than bacteria and they attach themselves to another living cell and use that cells' genetic material to reproduce themselves. Most viruses cause disease. Examples of diseases caused by viruses include the common cold, herpes, shingles, measles, chickenpox, COVID-19 and AIDS.
Antibiotics will not treat a viral infection. Viral infections require either vaccinations to prevent them in the first place or antiviral drugs to inhibit their development.
Viruses are tinier than bacteria. In fact, the largest virus is smaller than the smallest bacterium. All viruses have is a protein coat and a core of genetic material, either RNA or DNA. Unlike bacteria, viruses can't survive without a host. They can only reproduce by attaching themselves to cells. In most cases, they reprogram the cells to make new viruses until the cells burst and die. In other cases, they turn normal cells into malignant or cancerous cells.
Also unlike bacteria, most viruses do cause disease, and they're quite specific about the cells they attack. For example, certain viruses attack cells in the liver, respiratory system, or blood. In some cases, viruses target bacteria.
The nasal cavity refers to the interior of the nose or the structure which opens exteriorly at the nostrils. It is the entry point for inspired air and the first of a series of structures which form the respiratory system. The cavity is entirely lined by the nasal mucosa, one of the anatomical structures (others include skin, body encasements like the skull and non-nasal mucosae such as those of the vagina and bowel) which form the physical barriers of the body’s immune system. These barriers provide mechanical protection from the invasion of infectious and allergenic pathogens.
Humans can smell thousands—perhaps even millions—of different scents. Yet scientists know that in the nose, there are only about 400 different types of odour receptors—proteins that capture scented molecules so that smells can be identified. Thus, there isn’t, obviously, one type of receptor that responds to a rose, while another jumps for jasmine.
So how can we smell so much, with so few types of receptors?
The answer is that cells mix and match. Each nerve cell in the nose can sense more than one odour but picks up the smell to a different degree. An odour's unique signature depends on which cells respond to it, and how intensely.
What happens when you inhale a rose is that a group of cells is stimulated, and that group sends a combination of signals to the olfactory bulb—the site at the very front of the brain where smell perception takes place. This unique combination of signals tells the brain the odour is the smell of a rose.
What are the different types of cells in the nose
The epithelium of the nasal mucosa is of two types – respiratory epithelium, and olfactory epithelium differing according to its functions. In the respiratory region, it is columnar and ciliated. Interspersed among the columnar cells are goblet or mucin cells, while between their bases are found smaller pyramidal cells.
The average number of viral particles needed to establish infection is known as the infectious dose. We don’t know what this is for covid-19 yet, but given how rapidly the disease is spreading, it is likely to be relatively low – in the region of a few hundred or thousand particles, says Willem van Schaik at the University of Birmingham, UK.
Viral load, on the other hand, relates to the number of viral particles being carried by an infected individual and shed into their environment. “The viral load is a measure of how bright the fire is burning in an individual, whereas the infectious dose is the spark that gets that fire going,” says Edward Parker at the London School of Hygiene and Tropical Medicine.
If you have a high viral load, you are more likely to infect other people, because you may be shedding more virus particles. However, in the case of covid-19, it doesn’t necessarily follow that a higher viral load will lead to more severe symptoms.
For instance, health workers investigating the covid-19 outbreak in the Lombardy region of Italy looked at more than 5,000 infected people and found no difference in viral load between those with symptoms and those without. They reached this conclusion after tracing people who had been in contact with someone known to be infected with the coronavirus and testing them to see if they were also infected.
Similarly, when doctors at the Guangzhou Eighth People’s Hospital in China took repeated throat swabs from 94 covid-19 patients, starting on the day they became ill and finishing when they cleared the virus, they found no obvious difference in viral load between milder cases and those who developed more severe symptoms.
Although it is difficult to draw firm conclusions at this stage, such studies “may impact our assumptions about whether a high number of viral particles predisposes to a more serious disease”, says van Schaik.ring the "dose" of coronavirus one can get, and its connection to the severity of COVID-19
Some young healthcare workers with a serious disease -- a result of a big viral dose?
But three questions deserve particular attention because their answers could change the way we isolate, treat, and manage patients.
First, what we can learn from the "dose-response curve" for the initial infection --- that is, can we quantify the increase of the risk of infection as people are exposed to higher doses of the virus?
Second, there is a relationship between the initial "dose" of the virus and the severity of the disease - that is, does more exposure result in graver illness?
And third, are the quantitative measures of how the virus behaves in infected patients (e.g. the peak of your body's viral load, the patterns of its rise and fall) that predict the severity of their illness and how infectious they are to others?
So far, in the early phases of the COVID19 pandemic, we have been measuring the spread of the virus across people. As the pace of the pandemic escalates, we also need to start measuring the virus within people.
Viruses
are small obligate intracellular parasites which by definition
contain either a
RNA a or DNA genome, surrounded by a protective virus –
coded protein coat.Edward
Jenner (1798) introduced the term virus in
microbiology. Virus
Greek means ‘’ poison’’. In
1892 for the first time a
Russian botanist DMITRI IWANOWSKI discover the virus. They are infectious and cause various diseases to host organism. They come in different shapes. Based on the types of host cells or organisms, there are different types of viruses as plant viruses, animal viruses, bacteriophages, fungal viruses, protists viruses, etc. However, this article mainly focuses on the difference between plant virus and animal virus.
SHAPE
Viruses are of different shapes such as spherical or cuboid ( adenovirus),
Variable size
from 20 nm to 300 nm in diameter. They
are smallest than bacteria,
some are slightly larger than protein and nucleic
acid molecules and some are
about of the same size ( smallpox virus) as the
smallest bacterium and some
virus slightly large (300 – 400 nm).
HELICAL
( CYLINDRICAL) VIRUSES
The
helical viruses are elongated, rod-shaped, rigid or flexible. There the capsid is a hollow cylinder with a helical structure. Capsid
consists of monomers arranged helically in the rotational axis. The
consist may be naked e.g. TMV or envelope e.g. influenza virus.
POLYHEDRAL (ICOSAHEDRAL) VIRUSES
Polyhedral the structure has the three possible symmetries such as
tetrahedral, octahedral and
icosahedral.
The
viruses are more or less spherical, therefore icosahedral symmetry is
the best
one for packaging and bonding of subunits. The
cap Somers of each
face form an equatorial triangle and 12 intercepting point
or corners.
They
consist of naked capsid e.g. adenovirus or envelope e.g. herpes simplex virus.
COMPLEX
VIRUSES
The
viruses which have the unidentifiable capsids or have the capsids with
additional structures are called complex viruses. Capsids
not clearly identified
e.g. vaccinia virus etc. Capsids to which some other the structure is attached
e.g. some bacteriophages etc.
ENVELOPE There are certain plant and animal viruses and bacteriophage both
icosahedral and helical, which are surrounded by a thin membranous envelope.
This envelope is about 10-15 µm thick.
it is made up of protein, lipids and
carbohydrates. Which are combined to form
glycoprotein and lipoprotein? Lipids provide flexibility to the shape, therefore viruses look of variable
size and shape. The protein component of the envelope is of viral origin and
lipid and carbohydrate may be the feature of the host membrane.
The key difference between plant virus and the animal virus is that the plant virus is an intracellular parasite that infects plants while the animal virus is an intracellular parasite that infects animal tissues. Plant Viruses
Plant viruses, like other viruses, contain a core of either
DNA or RNA. You have already learned about one of these,
The tobacco mosaic virus. As plants have a cell wall to protect their cells, these viruses do not use receptor-mediated endocytosis to enter host cells as is seen with animal viruses. For many plant viruses to be transferred from plant to plant, damage to some of the plants’ cells must occur to allow the virus to enter a new host.
This damage is often caused by weather, insects, animals,
fire, or human activities like farming or landscaping. Additionally,
plant offspring may inherit viral diseases from parent plants.
Plant viruses can be transmitted by a variety of vectors,
through contact with an infected plant’s sap, by living organisms such as insects and nematodes, and through pollen.
When plants viruses are transferred between different plants,
this is known as horizontal transmission, and when they are
inherited from a parent, this is called vertical transmission.
Symptoms of viral diseases vary according to the virus and its host (see the table below). One common symptom is hyperplasia, the abnormal proliferation of cells that causes the appearance of plant tumours known as galls.
Other viruses induce hypoplasia, or decreased cell growth,
in the leaves of plants, causing thin, yellow areas to appear.
Still, other viruses affect the plant by directly killing plant cells,
a process is known as cell necrosis. Other symptoms of plant viruses
include malformed leaves, black streaks on the stems of the plants,
altered growth of stems, leaves, or fruits, and ring spots, which are
circular or linear areas of discolouration found in a leaf.
Plant viruses can seriously disrupt crop growth and development, significantly affecting our food supply. They are responsible for poor crop quality and quantity globally and can bring about huge economic losses annually. Others viruses may damage plants used in landscaping. Some viruses that infect agricultural food plants include the name of the plant they infect, such as tomato spotted wilt virus, bean common mosaic virus, and cucumber mosaic virus. In plants used for landscaping, two of the most common viruses are peony ring spot and rose mosaic virus. There are far too many plant viruses to discuss each in detail, but symptoms of bean common mosaic virus result in lowered bean production and stunted, unproductive plants. In the ornamental rose, the rose mosaic disease causes wavy yellow lines and coloured splotches on the leaves of the plant.
Animal Viruses
Animal viruses, unlike the viruses of plants and bacteria, do not
have to penetrate a cell wall to gain access to the host cell.
Non-enveloped or “naked” animal viruses may enter cells in two different ways. As a protein in the viral capsid binds to its receptor
on the host cell, the virus may be taken inside the cell via a
vesicle during the normal cell process of receptor-mediated
endocytosis. An alternative method of cell penetration used by non-enveloped viruses is for capsid proteins to undergo shape changes after binding to the receptor, creating channels in the host cell membrane. The viral genome is then “injected” into the host cell through these channels in a manner analogous to that used by many bacteriophages. Enveloped viruses also
have two ways of entering cells after binding to their receptors:
receptor-mediated endocytosis, or fusion. Many enveloped viruses enter the cell by receptor-mediated endocytosis in a
fashion similar to some non-enveloped viruses. On the other hand,
fusion only occurs with enveloped virions. These viruses, which include HIV among others, use special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm.
After
making their proteins and copying their genomes, animal viruses complete the
assembly of new viruses and exit the cell. As we have already discussed using
the example of HIV, enveloped animal viruses may bud from the cell the membrane
as they assemble themselves, taking a piece of
the
cell’s plasma membrane in the process. On the other hand, non-enveloped viral
progeny, such as rhinoviruses, accumulate in infected cells until there is a
signal for lysis or apoptosis and all viruses are released together. Animal
viruses are associated with a variety of human diseases.
Some of them follow the classic pattern of
acute disease, where symptoms get increasingly worse for a short period followed
by the elimination of the virus from the body by the immune system and eventual recovery from the infection.
Examples of acute viral
diseases
are the common cold and influenza. Other viruses cause long-term chronic
infections, such as the virus causing hepatitis C, whereas others, like herpes
simplex virus, only cause intermittent
symptoms. Still other viruses, such as human
herpesviruses 6 and 7, which in some cases can cause minor childhood disease
roseola, often successfully cause productive infections without causing any
symptoms
at all in the host, and thus we say these patients have an asymptomatic
infection.
In
hepatitis C infections, the virus grows and reproduces in liver cells, causing
low levels of liver damage.
The
damage is so low that infected individuals are often unaware that they are
infected, and many infections are detected only
by
routine blood work on patients with risk factors such as intravenous drug use. On the other hand, since
many of the symptoms
of viral diseases are caused by immune responses,
a lack of symptoms is an indication of a weak
immune response to the
virus. This allows the virus to escape elimination by the immune system and persist in individuals
for years, all the while producing low levels of progeny virions
in what is known
as a
chronic viral disease. Chronic infection of the liver by this
the
virus leads to a much greater chance of developing liver cancer,
sometimes
as much as 30 years after the initial infection.
As
already discussed, the herpes simplex virus can remain in a state of latency in
nervous tissue for months, even years.
As the
virus “hides” in the tissue and makes few if any viral proteins, there is
nothing for the immune response to act against, and immunity to the virus
slowly declines.
Under
certain conditions, including various types of physical and psychological
stress, the latent herpes simplex virus may be reactivated and undergo a lytic
replication cycle in the skin, causing the lesions associated with the disease.
Once
virions are produced in the skin and viral proteins are synthesized, the immune
response is again stimulated and resolves the skin lesions in a few days by
destroying viruses in the skin. As a result of this type of replicative cycle,
appearances of cold sores and genital herpes outbreaks only occur
intermittently,
even
though the viruses remain in the nervous tissue for life. Latent infections are
common with other herpesviruses as well, including the varicella-zoster virus
that causes chickenpox. Some animal-infecting viruses, including the hepatitis C
virus discussed above, are known as oncogenic viruses: They have the ability to
cause cancer. These viruses interfere with the normal regulation of the host
cell cycle either by
either
introducing genes that stimulate unregulated cell growth (oncogenes) or by
interfering with the expression of genes that inhibit cell growth. Oncogenic
viruses can be either DNA or RNA viruses.
Cancers
known to be associated with viral infections include cervical cancer caused by
human papillomavirus (HPV), liver cancer caused by hepatitis B virus, T-cell leukemia,
and several types of lymphoma. HPV, or human papillomavirus, has a naked
icosahedral capsid
visible
in this transmission electron micrograph and a double-stranded DNA genome that is
incorporated into the host DNA. The virus, which is sexually transmitted, is
oncogenic and can lead to cervical cancer.
What
are the Similarities Between Plant Virus and Animal Virus? Both plant virus and
animal virus are intracellular obligate parasites. They live within a host
cell. Moreover, they have either DNA or RNA genomes.Both types of viruses cause
various diseases.
Furthermore,
their genomes can either be single-stranded or double-stranded.
Also,
both can either be naked or enveloped.
What
is the Difference Between Plant Virus and Animal Virus?
