Understanding the Virosphere
Millions of years of evolution has caused
spectacular changes in our life,but what
remains a constant is the occurrence of diseases and viruses cause most of
them. In 1857 a strange contagious disease affecting up to 80 percent of the
tobacco crops. In 1879 plant pathologist Adolf Mayer named it the “ Mosaic
disease of tobacco”
In 1889 Dutch microbiologist Martinus W Beijerinck’s
findings say the disease agent needed growing leaves to multiply or to infect
other plants when he checked newly infected leaves,he found that with fresh
infections the disease agent did not lose its disease- causing power.His
conclusion was:the agent could grow on leaves but could not reproduce without
them. He named this agent “Contagious vivum fluidum” or contagious living
fluid. He also gave it a nickname,Viruses. Thus tobacco mosaic became the first
virus to be discovered.
The world of viruses is dense and vast. Its
diversity is greater than the world that we know and interect in. Viruses are
omnipresent,found in air,land,sea to every species to even in every body parts.
Virus disrupts cell function in its desperation to replicate. This makes us
sick. In response to infection the immune system springs into action white
blood cells,antibodies and other mechanisms go on an overdrive to rid the body
of the foreign invader. These cause fever,rash,headach and fatigue.
A disease occurs when the immune system loses ground to the viruses and
the later manages to establish itself in the cells for replication. The
replication process typically begins when a virus infects its host by attaching
to the host cell and penetrating the cell wall or membrane.
The virus genome is then uncoated
from the protein and hijacks the host cell’s machinery,forcing it to replicate
the viral genome and produce viral proteins to make new capsids. The new
viruses then burst out of the host cell during a process called lysis,which
kills the host cell. Some viruses take a portion of the host’s membrane during
the lysis process to form an envelope around the caspid. Following viral
replication the new viruses then go on to infect new hosts.
Most of the time body’s immune
system is capable enough to get rid of viruses. Problem arises when the virus
attacks the immune system to gain access to a cell and takes control over it .
These are the ones capable of causing outbreaks and sometimes pandemics.
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Viruses are microscopic parasites, generally much smaller than
bacteria.They lack the capacity to thrive and reproduce outside of a host
body.
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When a virus is completely assembled and capable of infection, it is
known as a virion. According to the authors of “Medical Microbiology 4th Ed.”
(University of Texas Medical Branch at Galveston, 1996), the structure of a
simple virion comprises of an inner nucleic acid core surrounded by an outer
casing of proteins known as the capsid. Capsids protect viral nucleic acids
from being chewed up and destroyed by special host cell enzymes called
nucleases. Some viruses have a second protective layer known as the envelope.
This layer is usually derived from the cell membrane of a host; little stolen
bits that are modified and repurposed for the virus to use.
The DNA or RNA found in the core of the
virus can be single stranded or double stranded. It constitutes the genome or the sum
total of a virus’s genetic information. Viral genomes are generally small in
size, coding only for essential proteins such as capsid proteins, enzymes, and
proteins necessary for replication within a host cell.
The
primary role of the virus or virion is to “deliver its DNA or RNA genome into
the host cell so that the genome can be expressed (transcribed and translated)
by the host cell,” according to "Medical Microbiology."
First, viruses need to access the inside of
a host’s body. Respiratory passages and open wounds can act as gateways for
viruses. Sometimes insects provide the mode of entry. Certain viruses will
hitch a ride in an insect’s saliva and enter the host’s body after the insect
bites. According to the authors of “Molecular Biology of the Cell, 4th Ed”
(Garland Science, 2002) such viruses can replicate inside both insect and host
cells, ensuring a smooth transition from one to the other. Examples include the
viruses that cause yellow fever and dengue fever.
Viruses
will then attach themselves to host cell surfaces. They do so by recognizing
and binding to cell surface receptors, like two interlocking puzzle pieces.
Many different viruses can bind to the same receptor and a single virus can
bind different cell surface receptors. While viruses use them to their
advantage, cell surface receptors are actually designed to serve the
cell.
After a virus binds to the surface of the
host cell, it can start to move across the outer covering or membrane of the
host cell. There are many different
modes of entry. HIV, a virus with an envelope, fuses with the
membrane and is pushed through. Another enveloped virus, the influenza virus,
is engulfed by the cell. Some non-enveloped viruses, such as the polio virus,
create a porous channel of entry and burrow through the membrane.
Once
inside, viruses release their genomes and also disrupt or hijack various parts
of the cellular machinery. Viral genomes direct host cells to ultimately
produce viral proteins (many a time halting the synthesis of any RNA and
proteins that the host cell can use). Ultimately, viruses stack the deck in
their favor, both inside the host cell and within the host itself by creating
conditions that allow for them to spread. For example, when suffering from the
common cold, one sneeze emits 20,000 droplets containing rhinovirus or
coronavirus particles, according to "Molecular Biology of the Cell."
Touching or breathing those droplets in, is all it takes for a cold to spread.
The recent emergence of the novel coronavirus
behind the COVID-19 pandemic throws a spotlight on the risks animals can pose
to humans as the source of new viruses. The virus in question, known as
SARS-CoV-2, was linked to a “wet market” for
wild animal trade in Wuhan, China, although it’s by no means
certain this was the source of the human version of the virus.
Bats were
identified as the animal with the closest known equivalent
virus although, again, we’re not sure that a bat provided the direct origin of
SARS-CoV-2.
So how do new viruses
actually emerge from the environment and start infecting humans? Every virus
has a unique origin in terms of its timing and mechanism, but there are some
general facts that are true for all species of emerging virus.
The first thing to
know is that it is rare for viruses to jump between species. In order for a
virus to successfully jump into a
new species of host, it must be able to do several things.
First, it must be
able to establish an infection in the new host by replicating itself there.
This is not a given, as many viruses can only infect specific types of cells,
such as lung cells or kidney cells. When attacking a cell, a virus binds to
specific receptor molecules on the cell’s surface and so may not be able to
bind to other types of cell. Or the virus may simply be unable to replicate
inside the cell for whatever reason.
Once it has infected
a new host, the virus must also be able to replicate itself enough to infect
others and transmit itself to them. This, again, is very rare and most virus
jumps will result in what we call “dead-end hosts” from which the virus cannot
transmit itself and eventually dies.
For example, the
influenza virus H5N1, or ‘bird flu’ can infect humans from
birds, but has very limited transmission between humans. Occasionally, this
barrier is overcome, and the emerging virus is able to jump to a new host,
establishing a new transmission chain and a novel outbreak.
From research over the past few decades, we understand some of the
mechanisms that contribute to virus jumps between species. Influenza virus is a
classic example. The virus contains eight genome segments and if two different
viruses infect the same cell, segments from both can mix to create a novel
virus species. If the proteins on the surface of the new virus have
significantly changed from currently circulating influenza virus strains, then
no one will have immunity and the new virus can easily spread.
This shift in the influenza virus is called antigenic
shift. This is what we think
happened with the 2009 H1N1 influenza epidemic, with the shift
occurring in pigs and then jumping to humans to start the outbreak. There is
also genetic evidence that this mechanism can
occur in coronaviruses, although its role in the emergence of SARS-CoV-2
remains to be determined.
New viruses can also emerge through genetic mutations
within the virus genome, which are more common among viruses that, instead of
deoxyribonucleic acid (DNA), store their genetic information in the similar
molecule Ribonucleic acid (RNA). This is because these viruses (with the
exception of coronaviruses) lack a way to check for mistakes when they
replicate. Most of the mutations produced during replication will be damaging
to the virus but some will enable it to infect a new host more effectively.
New coronavirus
So what do we think happened in the case of SARS-CoV-2?
Recent analysis of the genome suggest that the virus had been circulating in a
very similar form to today for approximately 40 years. The closest relative of
the virus that we can identify is one found in bats. However, this virus and
SARS-CoV-2 probably shared a common ancestor approximately 40-70 years ago, and
so this bat virus is not the cause of the outbreak.
Although these viruses share a common ancestor, 40 years
of evolution since then has separated them. This means that SARS-CoV-2 may have
jumped to humans from bats, or it may have come via an intermediate species.
Closely related viruses have been found in pangolins, for example. But the exact
path of the genetically distinct SARS-CoV-2 will remain a mystery until we are
able to find closer relative species in the environment.
It is also unclear what changed in the virus to allow it
to infect humans so easily. However, given that three major diseases have
emerged from the coronavirus family in the last 20 years – Severe acute
respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and
COVID-19 – it is likely that this will not be the last time a coronavirus jumps
into humans and causes a new disease outbreak.
What makes this more likely is that while they circulate
in all animals in the world, viruses are only able to jump to humans when they
have an opportunity from contact between us and other animals. Humans have always come
into contact with new viruses as they have explored new areas and spread across
the globe. But increased human activity in wild areas and the trade in wild
animals creates a perfect breeding ground.
This is also compounded by our global connectedness, which enables
a new disease to spread around the world in days. We
must accept some responsibility for these emergence events as we continue to
disturb natural environments and increase the likelihood of viruses jumping
into humans.
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The fact that the host range — the group of
cell types that a virus can
infect — is generally restricted serves as a basis for classifying viruses. A
virus that infects only bacteria is called a bacteriophage,
or simply a phage.
Viruses that infect animal or plant cells are referred to generally
as animal viruses or plant viruses. A few viruses can
grow in both plants and the insects that feed on them. The highly mobile
insects serve as vectors for transferring such viruses between susceptible
plant hosts. An example is potato yellow dwarf virus, which can grow in
leafhoppers (insects that feed on potato plant leaves) as well as in potato
plants. Wide host ranges are characteristic of some strictly animal viruses,
such as vesicular stomatitis virus, which grows in insects and in many
different types of mammalian cells. Most animal viruses, however, do not
cross phyla, and some (e.g., poliovirus) infect only closely related species
such as primates. The host-cell range of some animal viruses is further
restricted to a limited number of cell types because only these cells have
appropriate surface receptors to which the virions can attach.
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सरकारी विद्यालयों में 2005 से मध्याह्न भोजन योजना को संगठित तौर से प्रारंभ किया गया है। मध्याह्न भोजन संचालन की जिम्मेदारी विद्यालय के प्रधानाध्यापक की होती है लेकिन प्रबंधन विद्यालय शिक्षा समिति की देखरेख में किया जाता है। पोषण की प्रतीपूर्ती के लिए प्रतिदिन बिहार के 70 हजार 238 विद्यालयों में 1 करोड़ 30 लाख बच्चों को 1 लाख 68 हजार रसोईया खाना खिलाते हैं। बच्चों को सभी पोषक तत्व समुचित मात्रा में मिले इसके लिए प्रतिदिन का अलग-अलग मेन्यु निर्धारित है। छात्रों का स्वास्थ्य परीक्षण,डीवर्मिंग,आयरन-फोलिक की गोली का वितरण बिना किसी भेद-भाव के किया जाता है। गुरू-शिष्य परंपरा के तहत ऐसी जवाबदेही आश्रम के ऋषि-मुनियों की रहती थी। 
