Viral diseases cause substantial losses in agricultural crops and livestock, directly affecting economies dependent on these sectors, such as cotton production in Pakistan.

Viral diseases like the Cotton Leaf Curl Virus and bird flu cause significant financial damage, making it essential to monitor and manage these diseases to protect the economy.

Pakistan contributes 4.55% of the total global raw cotton exports, emphasizing the importance of cotton production to its international trade and economy.

Bird flu caused an estimated economic loss of Rs. 700-800 million during its peak in 1992, showcasing the devastating impact of viral diseases on national economies.

The Cotton Leaf Curl Virus has severely impacted Pakistan's economy, causing a loss of Rs. 50-55 billion, underlining the need for vigilant measures to manage viral plant diseases.

Pakistan ranks fourth in the world in terms of cotton area, contributing 9.36% of the total global cotton area, highlighting the importance of cotton to its economy.

The measles virus spreads efficiently through airborne droplets and can remain infectious in the air for hours, making it highly contagious.

Coronavirus infections, particularly severe cases, are characterized by labored breathing, chest pain, low oxygen levels, and potential respiratory failure.

Coronavirus spreads via respiratory droplets from an infected person during coughing, sneezing, or close contact, making it a highly transmissible virus.

Measles presents with fever, cough, runny nose, and a characteristic rash, along with potential complications such as pneumonia in severe cases.

The measles virus spreads through airborne droplets released when an infected person coughs or sneezes, making it highly contagious.

The measles virus has a negative-sense single-stranded RNA genome, which requires conversion into a positive-sense strand for protein synthesis.

The Ebola virus is harbored by animals like bats, dogs, and canids, and transmission occurs through contact with infected body fluids or tissues.

Dengue virus infection causes flu-like symptoms, including high fever, rashes, pain behind the eyes, nausea, and vomiting, transmitted by Aedes mosquitoes.

Hepatitis C virus, a positive-sense single-stranded RNA virus, is commonly transmitted through infected blood during transfusions, causing symptoms like jaundice, fatigue, and muscle pain.

Ebola virus, a negative-sense single-stranded RNA virus, is transmitted through contact with the body fluids of infected animals or humans and causes hemorrhagic fever.

The Aedes mosquito is responsible for transmitting the Dengue virus, a positive-sense single-stranded RNA virus, leading to symptoms like rashes, vomiting, and pain behind the eyes.

Chikungunya virus infection typically causes headache, severe muscle and joint pain, nausea, vomiting, and swollen glands.

The Chikungunya virus is a positive-sense single-stranded RNA virus transmitted by Aedes mosquitoes and infects humans and nonhuman primates.

Viroids primarily infect plants, causing diseases and distorted growth. They do not affect protein synthesis but replicate and produce specific RNA molecules.

The Potato spindle tuber viroid was the first identified viroid. It is one of approximately 33 known species of viroids that infect plants.

Viroids utilize the host cell's RNA polymerase to replicate their RNA genome, even though they lack the ability to encode proteins.

The smallest viroid discovered so far is 220 nucleotides long, significantly smaller than most viruses, which can range up to thousands of bases.

Viroids are small infectious agents composed of single-stranded RNA. They lack a protein coat and are smaller and simpler than viruses.

Prions are stabilized by a single disulfide bond, making them resistant to denaturation and enabling their persistence in harsh environmental conditions.

Unlike viruses and other pathogens, prions are entirely protein-based and do not contain any nucleic acids, such as DNA or RNA.

Prions are linked to several neurological disorders in humans, including Alzheimer's disease, insomnia (fatal familial insomnia), and Trisomy 21.

Prions are composed of 29 amino acids with a single disulfide bond, making them highly stable and resistant to standard sterilization methods.

Prions are responsible for causing mad cow disease in cattle, along with other neurodegenerative diseases in humans, such as Creutzfeldt-Jakob disease.

Prions are infectious agents made entirely of protein molecules. They lack nucleic acids and are associated with neurodegenerative diseases.

Cotton Leaf Disease caused by Begomovirus can be managed by using sprays to kill vector pests like whiteflies and by burning infected plants to prevent spread.

Polio affects the nervous system, leading to symptoms such as paralysis, headache, fever, and body pain.

Polio spreads through fecal-oral transmission, typically via contaminated water or food, affecting the nervous system and potentially causing paralysis.

Herpes simplex virus causes painful sores and fever blisters around the mouth, genitals, and anus, along with flu-like symptoms.

Preventing Hepatitis includes proper hand hygiene, avoiding contaminated food and water, and avoiding contact with infected bodily fluids.

Hepatitis is caused by the Hepatitis virus and often leads to yellowing of the skin and urine, fatigue, pain in the abdomen, and loss of appetite.

HIV spreads through unprotected sexual contact, contaminated needles, blood transfusions, and from mother to child during pregnancy or breastfeeding.

Drugs like Rukobia, Descovy, and Truvada are part of ART, specifically targeting viral enzymes to suppress HIV replication and manage the infection.

HIV detection involves tests like antibody tests and nucleic acid tests (NATs) to confirm the presence of the virus in blood or saliva samples.

ART involves a combination of drugs that target different stages of the HIV life cycle, such as inhibiting viral enzymes, to control the infection and slow disease progression.

As HIV progresses to AIDS, the destruction of T lymphocytes weakens the immune system, leading to opportunistic infections such as tuberculosis, pneumonia, and certain cancers like Kaposi's sarcoma.

In the asymptomatic stage, which can last up to ten years, the virus continues replicating and weakening the immune system, even though no symptoms are evident.

Early symptoms of HIV include fever, flu-like symptoms, and headache. These symptoms typically appear within the first six weeks of infection before progressing to the asymptomatic phase.

HIV hijacks the host cell’s ribosomes to translate viral mRNA into proteins necessary for assembling new viral particles, parasitizing the host cell's machinery.

During the budding stage, new HIV particles are released from the host cell by pinching off from the cell membrane, taking part of the host’s lipid bilayer as their envelope.

By destroying Helper T cells, HIV weakens the immune system's ability to coordinate responses, such as activating B cells for antibody production and cytotoxic T cells to eliminate infected cells.

The glycoprotein gp120 on HIV acts like a "lock and key," binding specifically to CD4 receptors on Helper T cells, which enables the virus to enter and infect these cells.

HIV uses gp120 glycoproteins on its surface to bind to CD4 receptors and co-receptors on host Helper T cells, initiating cell entry through endocytosis.

HIV specifically targets CD4+ Helper T lymphocytes, which are crucial for coordinating the immune response by activating other immune cells like cytotoxic T cells and B cells.

During transcription, the integrated viral DNA produces mRNA, which is translated into viral proteins necessary for the assembly of new viruses.

HIV integrates its DNA into the host genome, where it can remain inactive for years, avoiding immune detection and reactivating under specific conditions.

In the budding step, newly formed HIV particles are released from the host cell, acquiring a lipid envelope from the host cell membrane in the process.

During integration, the viral DNA synthesized by reverse transcriptase is inserted into the host's DNA using the enzyme integrase, allowing the virus to use the host machinery for replication.

HIV uses glycoproteins gp120 and gp41 to bind to CD4 receptors and co-receptors on host lymphocyte cells, facilitating virus entry.

Reverse transcriptase is an enzyme in HIV that converts its RNA genome into DNA, enabling integration into the host cell’s DNA for replication.

HIV contains two single-stranded RNA molecules as its genetic material, which are enclosed in a protein capsid and surrounded by a lipid envelope.

Genetically modified bacteriophages are used to attack and destroy pathogenic bacteria in the body, offering an alternative treatment for bacterial infections.

Bacteriophages are highly host-specific and target only the pathogenic bacteria they are designed to infect, leaving other beneficial microbes and host cells unharmed.

Bacteriophages can present antigens that activate the immune system, helping the body identify and eliminate pathogenic bacteria.

Genetically modified bacteriophages specifically attack and destroy pathogenic bacteria while being harmless to other cells and microbes, making them effective and safe therapeutic agents.

Bacteriophages are used in genetic engineering as vectors to transfer required genes from one cell to another, enabling the production of valuable products or genetic modifications.

The lysogenic cycle enables the bacteriophage to replicate its genetic material passively with the host cell's DNA, ensuring survival without killing the host cell.

In the lytic cycle, the viral genome directs the synthesis of new viral particles, causing the host cell to lyse and release the newly formed viruses.

During the prophage phase, the viral genome integrates into the host DNA and remains dormant, replicating passively with the host genome without harming the cell.

Environmental factors like radiation or chemicals can stimulate the prophage to become active, excise itself from the host DNA, and enter the lytic cycle, leading to the production of new viruses.

A prophage is the viral DNA that is incorporated into the bacterial genome during the lysogenic cycle. It remains dormant and replicates with the host DNA.

In the lysogenic cycle, the viral DNA becomes part of the host's DNA, forming a prophage, and replicates passively with the host genome without killing the cell.

During replication, the phage DNA takes over the host cell's machinery to produce viral proteins and nucleotides, which are necessary for creating new viral particles.

In the maturation phase, newly synthesized viral components, including DNA and proteins, assemble to form complete phage particles.

Lysozyme is an enzyme released by the bacteriophage to break the bacterial cell wall, causing lysis and the release of newly formed bacteriophages.

In the genome penetration phase, the bacteriophage injects its DNA into the host bacterium after breaking through the bacterial cell wall.

Phage attachment is the initial step of the lytic cycle, where the bacteriophage binds specifically to the surface of the host bacterial cell.

In the lytic cycle, bacteriophages inject their DNA into the host bacterium, replicate using the host's cellular machinery, and eventually lyse the cell to release new phages.

The helical capsid of TMV completes about 130 turns per rod, creating its characteristic rod-like structure.

Each capsomere of TMV contains approximately 158 amino acids, which contribute to the structure and functionality of the viral capsid.

TMV has a helical arrangement of capsomeres, which spiral around the RNA genome to form a rod-like structure.

The capsid of TMV is formed by approximately 2,130 capsomere subunits, arranged helically around the RNA to provide structural stability.

The capsid is the protein coat of TMV that protects its RNA genome. It is composed of numerous protein subunits called capsomeres.

TMV is an RNA virus with a centrally located single-stranded RNA genome that serves as its genetic material, surrounded by a protein coat.

Tail fibers recognize and bind to specific receptor sites on the bacterial surface, ensuring the bacteriophage attaches only to compatible host cells.

The base plate has proteinaceous retractable pins that pierce the bacterial cell wall, creating a path for the viral DNA to enter the host cell.

The tail sheath contracts during infection, driving the tail tube through the bacterial cell wall and allowing the phage DNA to enter the host cytoplasm

Tail fibers extend from the base plate and play a critical role in identifying and attaching to specific receptor sites on the bacterial surface.

The base plate, located at the end of the tail, contains tail fibers that bind to specific receptors on the host cell, ensuring stable attachment for DNA injection.

The tail of a bacteriophage connects the head to the host cell and functions as a tube-like structure that facilitates the transfer of DNA into the host.

The head of a bacteriophage is polyhedral (icosahedral) and contains double-stranded DNA, which carries the genetic instructions for virus replication.

RNA is chemically less stable than DNA, making RNA viruses more susceptible to damage under extreme environmental conditions, such as high temperatures or UV exposure.

Lipid-enveloped viruses, such as influenza, are more sensitive to changes in relative humidity compared to non-lipid-enveloped viruses, as their lipid layer is prone to environmental degradation.

Airborne virus survival depends significantly on relative humidity. The percentage of water vapor in the air influences their stability, with lipid-enveloped viruses being more vulnerable at certain humidity levels.

Airborne viruses use expelled organic material, such as saliva or mucous, to shield themselves from environmental conditions, such as dryness or heat, during coughing or sneezing.

A temperature of 60°C or higher is usually sufficient to inactivate most viruses by damaging their nucleic acids or proteins.

High temperatures can denature viral proteins and dissociate capsids, inactivating viruses. DNA viruses are generally more resistant than RNA viruses to such damage.

Viruses can survive outside a host under favorable environmental conditions such as specific temperature and pH, maintaining their infectivity until they find a host.

Viruses frequently mutate and alter their genome to evade host immune responses, making treatments like vaccines less effective over time.

Viruses suppress B cell activation to inhibit the production of antibodies, preventing the immune system from effectively targeting and eliminating viral infections.

Viruses suppress the presentation of their antigens by MHC molecules, delaying the activation of helper T cells and the immune system's ability to respond.

Viruses block the interferon response by interrupting the production of proteins necessary for immune signaling, thereby allowing viral replication without interference from the immune system.

Viruses mimic host complement proteins, deactivating the complement system, which is a part of innate immunity. This helps viruses evade immune detection and replication interference.

Phage viruses synthesize endonuclease enzymes that degrade the bacterial DNA, enabling them to take over the host cell's replication and metabolic processes.

Viruses are obligate intracellular parasites, meaning they require a living host cell to provide the machinery and energy for replication and protein synthesis.

Viruses integrate their genetic material into the host genome or use the host's cellular machinery to force the cell to replicate viral components, overriding normal cellular processes.

Viruses contain nucleic acids (either DNA or RNA) as their genetic material. These nucleic acids direct the host cell to replicate the viral genome and produce new viral particles.

Viruses use the host cell's enzymes, organelles, and metabolic machinery to replicate their genome and produce proteins, as they lack the ability to do so on their own.

Viruses depend on host cells to replicate and produce proteins, as they lack the necessary machinery to carry out these processes independently. The host provides all vital functions required for the virus's survival.

Viruses are noncellular because they lack organelles, metabolic machinery, and the ability to generate energy or synthesize proteins independently. They require a host cell for replication and survival.

Reverse-transcribing viruses have a unique replication mechanism where their RNA genome is transcribed into DNA for integration into the host genome. Examples include HIV and Hepatitis B.

Single-stranded RNA viruses with a DNA intermediate, like HIV, use reverse transcriptase to form DNA, which is integrated into the host genome for further transcription and translation.

Hepatitis B virus has a double-stranded DNA genome and replicates using an RNA intermediate. It employs reverse transcription to replicate its genome.

Single-stranded RNA viruses with a DNA intermediate, such as retroviruses like HIV, have a positive-sense RNA genome. They convert RNA into DNA for integration into the host genome during replication.

Reverse-transcribing viruses, such as HIV, use the enzyme reverse transcriptase to convert their RNA genome into DNA, which integrates into the host genome for replication.

Negative-sense RNA viruses, like Rhabdoviruses and Paramyxoviruses, must synthesize a complementary mRNA strand from their RNA genome using host cell enzymes before translation can occur.

Reoviruses are double-stranded RNA viruses, while Dengue virus, Hepatitis C virus, and Coronaviruses are examples of positive-sense single-stranded RNA viruses.

In double-stranded RNA viruses, the mRNA is used for translating viral proteins and replicating the genome for producing new progeny.

Double-stranded RNA viruses use host cell enzymes to synthesize single-stranded mRNA, which serves as a template for protein synthesis and viral replication.

Positive-sense RNA viruses have genomes that are directly translated by the host's ribosomes into proteins without requiring any intermediate steps.

Positive-sense single-stranded RNA viruses, such as Coronaviruses, Dengue virus, and Hepatitis C virus, have RNA genomes that function directly as mRNA, allowing immediate translation in host cells.

Double-stranded RNA viruses have a genome made of two RNA strands. They use host cell enzymes to produce single-stranded mRNA for protein synthesis and replication. An example is Reoviruses.

David Baltimore classified viruses into groups based on their genome type (DNA or RNA, single-stranded or double-stranded) and their replication mechanisms.

Double-stranded RNA viruses use one strand of their RNA genome as a template to synthesize mRNA, which is then used for translation and replication.

Double-stranded RNA viruses, like Reoviruses, use their genome to produce single-stranded mRNA, which is translated into proteins and replicated within host cells.

Single-stranded DNA viruses must become double-stranded in the host cell before synthesizing mRNA to produce viral proteins and replicate.

Single-stranded DNA viruses, such as Parvoviruses, convert their single-stranded DNA to double-stranded DNA in host cells to synthesize mRNA.

CaMV is known for its circular capsid shape, differing from rod-like or spherical viruses.