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RNA viruses
Replicates in cytoplasm of host cell, require replicate to synthesize RNA from RNA. Replicase has a high mutation rate
Positive ssRNA
Ready for intermediate translation into proteins
Negative ssRNA
Needs to be converted into positive ssRNA to be made into proteins
dsRNA
Very rare genome, needs to be converted into positive ssRNA to be made into proteins
Retroviruses
Genome is positive ssRNA. Encode enzyme reverse transcriptase which makes negagive ssDNA from positive ssRNA. Complementary atrand synthezised to make dsDNA
Assembly
Capsomeres join together to begin creating the capsid, genome and enzymes packages in capsids to create nucleocapsids
Lysis
Two types. Virus incites host cell death, often used by naked viruses. Budding is when viral spike proteins insert into the host cell membrane, virus leaves cell, taking a part of the membrane with it, often used by enveloped viruses.
Naked viruses
Often release via lysis, causing tissue damage to host organism. More resistant to extreme ph, heat, dryness, simple disinfectants.
Enveloped viruses
Often release via budding, cells are long term “virus factories”. Envelope camouflages from host, more sensitive.
Influenza
Viral infection of respiratory tract, 4 types, type A is most common. Enveloped with segmented negative ssRNA. Spikes are embedded in envelope. Subtypes are based on their HA and NA
Anti-genetic drift
Minor mutations in HA and NA genes, often of a single amino acid. Mutations due to replicase, responsible for seasonal influenza
Antigenic shift
Concurrent infection allows mixture of 8 RNA segments, called reassortment. Uncommon. Human strain can gain novel HA and/or NA antigens, or animal strain can gain ability to infect humans
Latency
After penetration/uncoating, the viral genome goes latent (dormant) in one of two ways. Genome can exist separate from the host cell genome, or insert itself into the host genome. The viral genome now is replicated each time the host cell makes a new daughter cell. Viruses cycle from productive infection and latency
Acute infection
No latency, productive infection only. Rapid onset and short duration host may develop long laating immunity
Persistant infections
Viral genome is always in the body, release from infected cell via budding. Continues for years or lifetime. Three types of persistant infections are latent, chronic and slow
Latent infections
Infection is followed by symptomless non infectious period, then reactivation. Infectious particles not detected untill reactivation. Symptoms of initial and reactivation may differ
Chickenpox
Caused by varicella zoster virus. Itchy, blister like rash, fever, headaches, or severe complications. More severe in adults than in children. Highly contagious
Shingles
Caused by varicella zoster virus staying in the host after chickenpox going latent. Occurs when the virus reactivates later in life. Single stripe of blisters that wraps around either the left or right side of the body, ongoing nerve pain called postheraptic neuralgia. Pain may last for years
Chronic infections
Infectious virus can be detected at all times, signs and symptoms may come and go. Includes hepatitis b and c
Hepatitis
Each virus in completely different, only share the fact that they cause hepatitis. 20% of infections result in death from cirrhosis or liver cancer, most remain asymptomatic until near death.
Slow infections
Infectious virus gradually increases in amount over long period of time, no significant symptoms appear until it is fatal. Often capable of causing caner. (Ex-HIV)
How do viruses cause cancer?
Through a persistent infection that often induces latency. The virus can contain genes that promote cell overgrowth, or host cells have genes that moderate cell division and growth. Viral genome integrates into host cell genome during latency, interrupting important genes. Leads to uncontrolled growth. Usually caused by dsDNA viruses
Cytopathic effects (CPE)
Virus induced damage to the host cell that alters its microscopic appearance. Major changes in shape, develop intracelluar damage
Syncytium
Single large cell containing multiple nuclei, fusion of multiple host cells
RSV
Respiratory syncytial virus, causes infections of lungs and respiratory track. Very common, mild symptoms in older healthy children and adults. Prevented with antibodies in infants or vaccines
Bacterial viruses
Bacteriophages, have two types, lytic phages (t4) and temperate phages (lambda phage) shape is called complex, has a icosahedral nucleocapsid head and helical tail. Most genomes are dsDNA
Lytic phages
Preform a 5 step process for a productive infection called the lytic cycle. Attachment, genome entry, synthesis, assembly, release
Genome entry
Only the Bacteriophages viral genome in injected into the host cells cytoplasm
Temperate phages
may switch between lytic and lysogenic cycles. Lysogeny results in phage DNA becoming incorporated into the bacterial chromosome, with the viral DNA becoming a prophage. It is replicated when the host cell replicates
Transduction
Horizontal gene transfer, dna may be transferred by a bacteriophage from one bacterial cell to another
Viroids
Circular ssRNA that does not code for proteins. Has no capsid unlike viruses, infect flowering plants.
Prions
Proteinaceous infectious agents, composed of a misfolded protein without nucleic acids. Abnormal prions are more stable than normal ones that are apart of the CNS. When a bad prion finds a normal prion, the normal one refolds into a bad one. Cause diseases
Prion diseases
Progressive and fatal with no treatment. Prion proteins accumulate in neural tissue, neurons die, tissues develop holes, brain function deteriorates. From spontaneous genetic mutation, inherited gene that causes likely abnormal folding, introduction of a abnormal prion from a outside source
Variant creutzfeldt jakob disease
Rare and fatal disease that infects a person for many years before making them sick by destroying brain cells. Main cause is eating a product contaminated with infectious agent bovine spongiform encephalopathy (BSE) AKA mad cow disease.