Arboviruses are a diverse group of viruses transmitted by arthropods, causing illnesses ranging from mild fevers to severe diseases like encephalitis. They are classified mainly into three families: flaviviridae, togaviridae, and bunyaviridae, each associated with specific infectious diseases in humans. Prevention includes avoiding bites, vaccination, and vector control, though challenges in studying and cultivating these viruses persist due to their fastidious nature and ability to mutate.

1. Arboviruses are a group of viruses that are transmitted to humans and other animals by
mosquitoes, ticks, or other arthropods. The name "arbovirus" is an abbreviation of "arthropod-
borne virus". Arboviruses are found all over the world, and they can cause a wide range of
diseases, from mild fevers to serious encephalitis (inflammation of the brain).
Classification of arboviruses
Arboviruses are classified into several families and genera, based on their physical and genetic
properties. The three main families of arboviruses are:
• Flaviviridae: This family includes the viruses that cause yellow fever, dengue fever,
Zika virus disease, and West Nile virus disease.
• Togaviridae: This family includes the viruses that cause chikungunya virus disease,
eastern equine encephalitis, and western equine encephalitis.
• Bunyaviridae: This family includes the viruses that cause Rift Valley fever, Hantavirus
pulmonary syndrome, and California encephalitis.
In addition to these three families, there are a number of other families of arboviruses that are
less common.
Transmission of arboviruses
Arboviruses are transmitted to humans and other animals through the bite of an infected
arthropod. The arthropod becomes infected when it bites an animal that is already infected with
the virus. The virus then multiplies in the arthropod's body and is transmitted to the next animal
that the arthropod bites.
The transmission of arboviruses can be seasonal, depending on the climate and the life cycle
of the arthropod vector. For example, mosquitoes that transmit West Nile virus are most active
during the summer months.
Prevention and control of arboviral diseases
There are a number of ways to prevent and control arboviral diseases. These include:
• Avoiding mosquito and tick bites: This can be done by wearing long sleeves and pants,
using insect repellent, and staying indoors during peak mosquito and tick hours.
• Vaccination: There are vaccines available for some arboviral diseases, such as yellow
fever and Japanese encephalitis.
• Vector control: This involves controlling the populations of mosquitoes and ticks that
transmit arboviruses. This can be done by draining standing water, using pesticides, and
removing breeding sites for mosquitoes and ticks.

2. Flaviviruses
Flaviviruses are a family of enveloped viruses that are spherical in shape and have a diameter
of about 40-50 nanometers. They have a single-stranded RNA genome that is enclosed in a
lipid envelope. The envelope is derived from the host cell membrane and is covered with
glycoprotein spikes. The spikes are involved in the attachment and entry of the virus into host
cells.The morphology of different types of flaviviruses is generally similar, but there can be
some minor variations. For example, the size of the virus particles can vary slightly, and the
number and arrangement of the glycoprotein spikes can also vary.
FLAVIVIRIDAE
MORPHOLOGY
Here are some of the different types of flaviviruses and their morphology:
• Yellow fever virus: This virus is the prototype of the Flaviviridae family. It is about
45 nanometers in diameter and has a single-stranded RNA genome of about 10,700
nucleotides. The envelope of the virus is covered with glycoprotein spikes that are about
5 nanometers long.
• Dengue virus: This virus is closely related to yellow fever virus. It is about 40
nanometers in diameter and has a single-stranded RNA genome of about 11,000
nucleotides. The envelope of the virus is covered with glycoprotein spikes that are about
4 nanometers long.
• Zika virus: This virus is a newly emerging flavivirus. It is about 40 nanometers in
diameter and has a single-stranded RNA genome of about 11,400 nucleotides. The
envelope of the virus is covered with glycoprotein spikes that are about 4 nanometers
long.
• West Nile virus: This virus is found in many parts of the world, including North
America, Europe, and Africa. It is about 45 nanometers in diameter and has a single-
stranded RNA genome of about 11,200 nucleotides. The envelope of the virus is
covered with glycoprotein spikes that are about 5 nanometers long.
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3. REPLICATION
The replication of flaviviruses is a complex process that occurs in two main stages:
1. Entry and translation: The virus attaches to the host cell membrane through its
glycoprotein spikes. The virus then enters the cell by endocytosis. Once inside the cell,
the viral RNA is translated into a single polyprotein.
2. Genome replication and protein synthesis: The polyprotein is cleaved by viral and
cellular proteases into 10 different proteins. These proteins are responsible for a variety
of functions, including genome replication, protein synthesis, and assembly of new
virus particles.
The replication of flaviviruses is tightly regulated by a number of factors, including the host
cell environment, the availability of nutrients, and the presence of antiviral defenses.
The following are some of the key steps involved in the replication of flaviviruses:
1. Attachment and entry: The virus attaches to the host cell membrane through its
glycoprotein spikes. The virus then enters the cell by endocytosis.
2. Uncoating: The virus uncoats inside the cell, releasing the viral RNA.
3. Translation: The viral RNA is translated into a single polyprotein.
4. Cleavage of the polyprotein: The polyprotein is cleaved by viral and cellular proteases
into 10 different proteins.
5. Genome replication: The viral RNA is replicated by the viral RNA-dependent RNA
polymerase (RdRp).
6. Protein synthesis: The viral proteins are synthesized by the host cell ribosomes.
7. Assembly of new virus particles: The new virus particles are assembled in the
cytoplasm of the host cell.
8. Release: The new virus particles are released from the host cell by budding.
The replication of flaviviruses can be inhibited by a number of antiviral drugs, including
ribavirin and interferon. However, there is no cure for flavivirus infections, and treatment is
usually supportive.
Here are some of the challenges in studying the replication of flaviviruses:
• The viruses are difficult to grow in cell culture.
• The viruses are highly mutable, which makes it difficult to develop effective vaccines
and antiviral drugs.
• The viruses can cause a wide range of diseases, which makes it difficult to study the
specific effects of viral replication on each disease.

4. CULTIVATION
The cultivation of flaviviruses can be challenging due to their fastidious nature and the need
for specific cell types and culture conditions. However, there are a number of different methods
that can be used to cultivate flaviviruses, including:
• Primary cell culture: Primary cell culture is the most common method for cultivating
flaviviruses. Primary cells are cells that have been freshly isolated from an organism.
They are often more susceptible to infection by viruses than cultured cells.
• Continuous cell line culture: Continuous cell lines are cells that have been grown in
culture for many generations and have become immortal. They are often less
susceptible to infection by viruses than primary cells.
• Baculovirus expression system: The baculovirus expression system is a method of
cultivating viruses in insect cells. The baculovirus is a virus that infects insects. It can
be used to express the genes of other viruses, including flaviviruses.
• Chimeric virus system: The chimeric virus system is a method of cultivating viruses in
mammalian cells. A chimeric virus is a virus that is made up of the genes of two
different viruses. In this case, the genes of a flavivirus are combined with the genes of
a virus that can infect mammalian cells.
The choice of cultivation method will depend on the specific flavivirus that is being studied.
The method that is most commonly used is primary cell culture. However, the baculovirus
expression system and the chimeric virus system can be used to cultivate flaviviruses that are
difficult to grow in cell culture.
The cultivation of flaviviruses is an important step in the study of these viruses. It allows
researchers to study the replication and pathogenesis of the viruses, and to develop vaccines
and antiviral drugs.
Here are some of the challenges in cultivating flaviviruses:
• The viruses are sensitive to changes in temperature, pH, and the presence of certain
chemicals.
• The viruses can be inactivated by light and heat.
• The viruses can be difficult to isolate from infected cells.
• The viruses can be difficult to purify.
Despite these challenges, there are a number of methods that can be used to cultivate
flaviviruses. This allows researchers to study these viruses and develop new ways to prevent
and treat flavivirus infections.

5. Flaviviridae is a family of viruses that includes several pathogenic members, some of which
are responsible for serious diseases in humans. Key examples of pathogenic flaviviruses
include:
1. Dengue Virus: Causes dengue fever, a mosquito-borne viral disease that can range
from mild to severe, including dengue hemorrhagic fever and dengue shock syndrome.
2. Zika Virus: Known for causing Zika fever, which can lead to birth defects
(microcephaly) in infants born to infected mothers and neurological complications in
adults.
3. Yellow Fever Virus: Causes yellow fever, a viral hemorrhagic fever that can be fatal
in severe cases.
4. West Nile Virus: Transmitted by mosquitoes, it can cause West Nile fever and, in some
cases, severe neurological diseases like encephalitis or meningitis.
5. Japanese Encephalitis Virus: Leads to Japanese encephalitis, an inflammation of the
brain that can be severe, especially in children.
6. Hepatitis C Virus: A major cause of chronic liver disease, including cirrhosis and liver
cancer.
7. Hepatitis G Virus (GB Virus C): Although less pathogenic than some other hepatitis
viruses, it can cause liver infections.

7. 1. Envelope: Togaviruses are enveloped viruses, which means they are enclosed by a lipid
bilayer membrane. This envelope is derived from the host cell's membrane during the
viral budding process.
2. Shape: Togaviruses have a spherical or roughly spherical shape. They are often
described as having an icosahedral symmetry, which means they have a roughly
spherical shape with 20 equilateral triangular faces.
3. Capsid: Beneath the lipid envelope, togaviruses have a protein capsid. The capsid is
icosahedral in shape, and it encases the viral genetic material.
4. Genome: Togaviruses possess a single-stranded, positive-sense RNA genome. This
RNA molecule carries the genetic information required for viral replication and protein
synthesis.
5. Spike Glycoproteins: Embedded in the lipid envelope are spike-like glycoproteins.
These glycoproteins protrude from the viral surface and play crucial roles in the virus's
lifecycle. They are responsible for binding to host an immune response.
6. Rubella Virus Example: Rubella virus, a well-known member of the Togaviridae
family, exemplifies these morphological features. When observed under an electron
microscope, rubella virus particles appear as spherical entities with a granular or
"pebbly" surface due to the presence of the glycoprotein spikes.
The replication of Togaviridae, a family of viruses that includes alphaviruses like the
chikungunya virus and rubiviruses like the rubella virus, follows a well-defined process. Here
are the key steps in the replication cycle of Togaviridae:
1. Attachment and Entry:
• The virus initially attaches to specific receptors on the surface of host cells. The
attachment is typically mediated by viral glycoproteins on the virus envelope.
• After attachment, the virus is taken up by endocytosis, where it is engulfed by
the host cell in a vesicle called an endosome.
2. Uncoating:
• Once inside the endosome, the low pH environment triggers a conformational
change in the viral glycoproteins. This change is essential for the virus to release
its genetic material into the host cell's cytoplasm.
3. Translation:
• The viral RNA is then translated by the host cell's ribosomes to produce viral
proteins. Togaviruses use a cap-independent mechanism for translation.
• The initial translation produces non-structural proteins that are crucial for
replication and transcription.
4. Replication and Transcription:
• Togaviruses replicate their RNA genome and transcribe subgenomic RNAs in
the cytoplasm. This process occurs within specialized replication complexes.
• Non-structural proteins produced earlier are involved in replicating the viral
genome.
5. Translation of Structural Proteins:
• As replication and transcription continue, the viral RNA is used to synthesize
both non-structural and structural proteins.
• The structural proteins include those that form the capsid and the envelope
glycoproteins.
6. Assembly:

8. • Newly synthesized structural proteins and replicated viral RNA come together
to form new viral particles in the host cell's cytoplasm.
7. Budding and Release:
• The newly assembled virions are transported to the host cell's plasma
membrane.
• Budding occurs at the plasma membrane, where the viral particles acquire their
lipid envelope.
• Mature virions are then released from the host cell by exocytosis, often without
causing immediate cell lysis.
8. Infection of New Cells:
• Released virions can infect neighboring cells, continuing the cycle of infection
and replication.
It's important to note that the replication of Togaviridae viruses, like many other RNA viruses,
can result in genetic variation and the emergence of viral variants. This genetic diversity can
impact the virus's virulence and ability to evade host immune responses, which is significant
for the development of vaccines and antiviral treatments.
The cultivation of Togaviridae viruses, such as alphaviruses and rubiviruses, typically involves
the use of laboratory techniques and specific host cells. Here are the key steps in the cultivation
of Togaviridae viruses:
1. Selecting Host Cells:
• Togaviruses require specific host cells to replicate. The choice of host cells
depends on the particular Togaviridae virus being studied. Common host cells
for alphaviruses include mammalian cells like Vero cells or BHK-21 cells,
while rubella virus can be cultured in various human and simian cell lines.
2. Inoculation:
• Host cells are grown in culture dishes or flasks and then inoculated with the
Togaviridae virus of interest. This inoculation is typically done using a virus
stock that contains a known amount of the virus.
3. Incubation:
• After inoculation, the culture is incubated at a specific temperature and under
controlled conditions that favor viral replication. Alphaviruses, for example,
often replicate well at temperatures around 37°C.
4. Observation and Monitoring:
• The progress of viral replication is monitored by observing changes in the host
cells and, in some cases, by testing the culture medium for the presence of viral
particles or RNA.
5. Harvesting Virus:
• Once a sufficient amount of viral replication has occurred, the culture medium
is harvested. This medium contains newly produced viral particles.
6. Purification:
• The harvested culture medium may undergo purification steps to concentrate
and purify the virus. This can involve techniques like ultracentrifugation and
filtration.
7. Quantification:
• The concentration of the virus is determined, often using methods such as
plaque assays (for quantifying infectious virus particles) or quantitative PCR
(for measuring viral RNA).

9. 8. Characterization:
• The cultivated virus can be further characterized using techniques like electron
microscopy, genetic sequencing, and serological assays to confirm its identity
and properties.
It's important to note that working with Togaviridae viruses, especially live infectious ones,
should be conducted in appropriate biosafety containment facilities to prevent accidental
release and infection of laboratory personnel.
Cultivating Togaviridae viruses is crucial for various research purposes, including the
development of vaccines, studying viral pathogenesis, and investigating potential antiviral
treatments.

10. BUNYAVIRIDAE
Bunyaviridae is a family of viruses that exhibits a distinctive morphology. The family includes
several important pathogens, such as hantaviruses, phleboviruses, and orthobunyaviruses. Here
are the key features of the morphology of Bunyaviridae viruses:
1. Size and Shape: Bunyaviruses are typically spherical or pleomorphic (irregularly
shaped) and are relatively small, with an average diameter ranging from approximately
80 to 120 nanometers.
2. Envelope: Bunyaviruses are enveloped viruses, which means they are surrounded by a
lipid bilayer membrane derived from the host cell's membrane. This lipid envelope
contains viral glycoproteins.
3. Genome: Bunyaviruses have a segmented, negative-sense RNA genome. Unlike some
other viruses, their genome is divided into multiple segments, typically three, each
coding for a different set of viral proteins.
4. Capsid: Beneath the lipid envelope, Bunyaviridae viruses have a helical nucleocapsid.
This nucleocapsid is formed by the negative-sense RNA segments tightly wrapped
around nucleoproteins (N proteins).
5. Spike Glycoproteins: Embedded in the lipid envelope are spike-like glycoproteins,
including Gn (glycoprotein N) and Gc (glycoprotein C). These glycoproteins play a
crucial role in the attachment of the virus to host cells and the entry of the virus into
host cells.
6. Hantavirus-Specific Feature: Some bunyaviruses in the hantavirus genus have an
additional structure called the "nucleocapsid ring" or "helical nucleocapsid." This
unique structure is found within the viral envelope and is a characteristic feature of
hantaviruses.