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73 Cards in this Set
- Front
- Back
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Viruses: Nucleic acid with a protein coat
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• RNA or DNA; 4 to 400 genes
• Virus genes that code for 3 main functions – Infection of a host cell – Redirection of host cell’s metabolism to the production of virus-specified macromolecules – Escape from the host cell • Size – 1nm to 30nm (bacteria is 1um) |
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Viruses - architecture
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• Most are based on the association of the negatively charged (anionic) nucleic acids with a surrounding coat
of positively charged (cationic proteins) • Capsid – outer coat -Comprised of capsomeres – Icosahedral – 20 faces, each an equilateral triangle, 12 vertices and 20 edges * ex epcote- extreamly stable structure that contains self assembling capsomeres * – Helical – capsomeres wound ina spiral and form a hollow core ~ Encloses either DNA or RNA |
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Viruses - envelopes
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• An outer membrane surrounding the nucleocapsid of some viruses
• Membrane is aquired when virus leaves host cell – therefore of host origin and comprised of phospholipid bilayer. • Virus places viral glycoprotein spikes • Responsible for viral infectivity – absorbs to host receptors • Transmitted by body secretions – not water or insects |
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Viruses - Specificity
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• Specificity exists at the level of:
– Host species – Organ – Tissue • Example: viruses of humans will not usually attach other species and intestinal viruses will not attach in the respiratory tract. – Few viruses attack multi organ (chickenpox) • Host receptors are those used for hormones or signaling I.e.,HIV - CD4 on Th cells |
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Viruses: Growth Cycle
1. Attachment |
virus collides randomly with sites on host cells (1/1000 are successful.
– Virus may have projections on capsid attaches to receptors on host cells |
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Viruses: Growth Cycle
2. Penetration |
entrance of virus into cell cytoplasm
– Viroplexis – non-specific engulfment of virus - Membrane fusion – with enveloped virues. Capsid remains on outside |
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Viruses: Growth Cycle
3. Uncoating |
removal of viral protein coat and release of genetic material
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Viruses: Growth Cycle
4. Synthesis |
early viral proteins
• Shut off host cell • Stimulate host DNA polymerase • Code for viral DNA or RNA replicating enzymes – Viral DNA replicates – Late viral proteins – code for viral capsid • Maturation – assembly of viral components ie., nucleic acid is packed into capsid (self assembly) • Release – viruses leave host cell by either – Budding – slow release over time – Burst by cell lysis |
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Oncogenic DNA Viruses
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– Adenoviridae
– Heresviridae – Poxviridae – Papovaviridae – Hepadnaviridae |
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Prions Infectious protiens
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• Inherited and transmissible by ingestion, transplant, & surgical instruments
• Spongiform encephalopathies: Sheep scrapie, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, fatal familial insomnia, Bovine Spongioform encephalitis) mad cow disease • PrPC, normal cellular prion protein, on cell surface |
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Cancer and Oncogenic Viruses
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• Oncogenic RNA viruses
– Retroviridae • Viral RNA is transcribed to DNA which can integrate into host DNA • HTLV 1 • HTLV 2 • Activated oncogenes transform normal cells into cancerous cells. • Transformed cells have increased growth, loss of contact inhibition, tumor specific transplant and T antigens. • The genetic material of oncogenic viruses becomes integrated into the host cell's DNA. |
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Growth of virus
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• Requires living cells
– Neonatal animals – Chick embryo – Tissue culture • Look for cytopathic effect (CPE) – plaques or holes in cell layer • Inclusion body formation (Herpes inclusions) • Viruses must be grown in living cells. – Bacteriophages form plaques on a lawn of bacteria. • Animal viruses may be grown in living animals or in embryonated eggs. |
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Growing Viruses
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• Animal and plants viruses may be grown in cell culture.
– Continuous cell lines may be maintained indefinitely. • Cytopathic effects • Serological tests – identifies viral disease – Detect antibodies against viruses in a patient – Use antibodies to identify viruses in neutralization tests, viral hemagglutination, and Western blot • Nucleic acids – RFLPs – PCR |
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Viral Pathogenesis
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• Entry into host
• Upper respiratory tract – inhalation • Hand contact with mucous membranes – eyes • Open wounds, mucous membranes- direct contact with infected material • Direct injection – insect vectors, needles, blood products – Replication at site of entry – cause local disease – Blood,lymph, neurons, - endothelial cells – rashes – LN – swollen LN – Nerves – encephalitis • Dormant – inactive – chicken pox • Slow viral disease – neurodegenerative • oncogenesis • Temperate phage – (prophage or provirus) incorporates genetic material into host cell • Vertical transmission – replicate with cells • Induction – xrays, carcinogens, other infections induce a lytic cycle |
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DNA, non-enveloped: Adenoviruses
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• The virion is icosahedral and has 252 capsomeres and 240 hexons; the 12 capsomeres at the vertices are pentons, containing a penton fiber. The virion is composed of 9 different polypeptides. Most of the antigens are on the outer capsid and all show hemagglutinating activity.
• 5-10% of pediatric respiratory disease is attributable to Adenovirus. Disease predominates in winter, spread is from person to person and most outbreaks are not epidemic. • Clinically, disease can be transmitted by droplet transfer from an infected person via the respiratory route – Acute febrile pharyngitis: affects infants and children and is difficult to distinguish from influenza, or the common cold. – Pharyngeal-conjunctival fever – Acute respiratory disease: military recruits, this disease produces fever, cough, pharyngitis and a skin rash. – Adenovirus pneumonia: Usually a complication of acute respiratory disease – conjunctivitis and gastroenteritis. |
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Human Papilloma Virus
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• There are over 100 viruses known as human papilloma viruses (HPVs.)
– They are common. One study found HPVs in 77% of HIV-positive women. HPVs are transmitted easily during sexual activity. – Condoms do not totally prevent transmission of HPVs. – HPVs can be transmitted from person to person by direct contact with infected areas that aren’t covered by a condom. Some HPVs cause common warts of the hands or feet. Infections of the hands and feet are usually not transmitted through sexual activity. • There is no easy way to tell if someone is infected with an HPV. People who don't have any signs or symptoms of HPV infection can transmit the infection. • Several types of HPV cause genital warts on the penis, vagina, and rectum. HPV can also cause problems in the mouth or on the tongue or lips. • Other types of HPV can cause abnormal cell growth known as dysplasia. Dysplasia can develop into cancers of the penis and anus, and cervical cancer in women. • Nov. 11, 2004 -- A vaccine that protects women against a common sexually transmitted infection that leads to cervical cancer is expected to be approved by 2006. • The results of a major clinical trial of the vaccine show that it was 100% effective in preventing persistent infection with two strains of the human papillomavirus (HPV) that account for the majority of cervical cancer cases. |
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Enveloped DNA virus: Herpesviruses
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• cause acute infections but they are also capable of latency. This can lead to recurrent infections, which are important to the mechanism of host to host transmission.
• HSV-1, HSV-2 and VZV are termed "neurotropic" while CMV and EBV are "lymphotropic", referring to the cell type in which the latent infection is established. • Some Herpesviruses have been associated with the production of cancers, providing the best evidence for a viral etiology for these diseases. • Acyclovir (a nucleoside analog) is kinda effective against HSV infections |
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Herpesviruses: HSV-1
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• Gingivostomatitis in which oral cavity vesicles or ulcers form. These lesions may recur frequently as "cold sores" (herpes labialis).
• herpetic keratitis, which may be serious if accompanied by conjunctivitis because this can lead to corneal scarring and blindness. • "whitlows" appears as lesions on the fingers. |
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Herpesviruses : HSV-2
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• Commonly referred to as genital herpes. This virus produces lesions on the genitals, urethra & bladder.
• Recurrence may be frequent. • In neonates, infection may be local or disseminated and has about 50% mortality if untreated. • HSV-2 may also cause meningitis or encephalitis. |
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Herpesviruses :VZV produces
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the disease varicella and zoster
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Varicella
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is commonly known as chickenpox.
• mild infection in children • serious in adults, occasionally progressing to pneumonia. |
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Zoster
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is commonly known as shingles and is a manifestation of varicella infection. Typically occurring in older individuals, the lesions are confined to skin areas innervated by sensory nerves of the dorsal ganglia, primarily in the thoracic and lumbar regions. These nervous tissues are thought to be the sight of latent infection by VZV.
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Herpesviruses: Varicella
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• Characterized by a skin rash appearing first on the head and trunk, and later on the extremities. The skin lesions progress from macules pustules to crusts. These lesions are not prone to scar.
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Herpesviruses: CMV
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• infections are often asymptomatic but when infection occurs in utero, cytomegalic inclusion disease may result.
• This condition is characterized by jaundice, hepatosplenomegaly and central nervous system disorder. • CMV may also produce a form of disease characterized by fever, fatigue and atypical lymphocytes (mono –like) |
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Herpesviruses: EBV
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• EBV is primarily responsible for infectious mononucleosis, characterized by fever, fatigue, malaise and pharyngitis.
• EBV latently infects B-cells, creating the potential for recurrence. • strong association between EBV and Burkitt's lymphoma in Africa and nasopharyngeal carcinoma in the Orient and Africa provides evidence for a viral etiology for some human cancers. |
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Hepatitis Viruses
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- inflamation of liver
• Clinical diagnosis depends on the symptomology, which may include fever, malaise, headache, dark-colored urine and jaundice. • Serology is the best method for determining infection. |
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Hepatitis A: Clinical presentation
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• Varies from subclinical and mild in children to jaundice in adults.
• The virus usually enters by intestinal infection (fecal-oral transmission), spreads via the blood to the liver, which is its target organ. • HAV is detectible in the feces during the incubation period (average 4 weeks), preceding a rise in serum levels of aminotransferase enzymes and the occurrence of pathologic changes in the liver. • Most disease resolves within two weeks |
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Hepatitis B: HBV
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• contains a circular, partly double-stranded DNA genome 3200 nucleotides in length.
• contains a DNA-dependent DNA polymerase and a reverse transcriptase and replicates via an RNA intermediate. • HBV possesses several antigens; the "Australian antigen" is associated with the surface (HBsAg), the "core antigen" (HBcAg) is internal and the "e antigen" (HBeAg) is part of the same capsid polypeptide as the HBcAg. All of these antigens elicit specific antibodies. |
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Hepatitis B: HBV pathogenesis
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• There are generally two patterns of HBV-associated disease:
1.Chronic persistent: Infections are generally asymptomatic with a mild elevation of serum alanine transaminase (ALT) and little liver fibrosis. 2.Chronic active: Infections produce jaundice with elevated ALT levels, liver damage and cirrhosis. Liver failure may predispose those affected to |
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Hepatitis
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• Hepatitis C: HCV may also produce a persistent carrier state, a higher level of chronic disease & cirrhosis.
• HCV infections result from blood transfusion. • Serum hepatitis (HBV, HCV) is generally passed via blood, unsterile syringes, transfusions, etc. A carrier state can occur; in North America and Europe, the rate is about 0.1%. The rate increases to about 25-30% in Africa, Asia and the Pacific. |
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Features of Hepatitis C Virus Infection
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• Incubation period Average 6-7 weeks
• Range 2-26 weeks • Acute illness (jaundice) Mild (<20%) • Case fatality rate Low • Chronic infection 60%-85% • Chronic hepatitis 10%-70% (most asx) • Cirrhosis <5%-20% • Mortality from CLD 1%-5% Agerelated |
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Exposures Known to Be Associated With HCV Infection in the United States
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• Injecting drug use
• Transfusion, transplant from infected donor • Occupational exposure to blood – Mostly needle sticks • Iatrogenic (unsafe injections) • Birth to HCV-infected mother • Sex with infected partner – Multiple sex partners |
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Injecting Drug Use and HCV Transmission
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• Highly efficient
– Contamination of drug paraphernalia, not just needles and syringes • Rapidly acquired after initiation – 30% prevalence after 3 years – >50% after 5 years • Four times more common than HIV |
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Occupational Transmission of HCV
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• Inefficient by occupational exposures
• Average incidence 1.8% following needle stick from HCV positive source – Associated with hollow-bore needles • Case reports of transmission from blood splash to eye; one from exposure to non-intact skin • Prevalence 1-2% among health care workers – Lower than adults in the general population – 10 times lower than for HBV infection • Recognized primarily in context of outbreaks – Chronic hemodialysis – Hospital inpatient setting – Private practice setting – Home therapy |
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Sexual Transmission of HCV
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• Occurs, but efficiency is low
– Rare between long-term steady partners – Factors that facilitate transmission between partners unknown (e.g., viral titer) – Low prevalence (1.5%) among long-term partners • infections might be due to common percutaneous exposures (e.g., drug use), BUT – Male to female transmission more efficient • more indicative of sexual transmission • Accounts for 15-20% of acute and chronic infections in the United States – Sex is a common behavior – Large chronic reservoir provides multiple opportunities for exposure to potentially infectious partners * Source: Sentinel Counties, CDC Sources of Infection for Persons With Hepatitis C * - Sexual 15% - Other 1%* - Unknown 10% - Injecting drug use 60% - Transfusion 10% (before screening) * Nosocomial; iatrogenic; perinatal - Occupational 4% |
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Poxviruses
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Variola virus (genus Orthopoxvirus
• dsDNA genome, have a complex morphology and replicate in the host cytoplasm. • Poxviruses cause localized and generalized infections in humans and animals. • Smallpox was the major human disease agent but it was officially declared eradicated by the World Health Organization (WHO) in 1980. • Smallpox is transmitted via the respiratory route. In the body, it is spread by a transient viremia to internal sites, and then a second viremia to the skin where the characteristic lesions erupt. • The lack of an animal reservoir made eradication of human disease possible. |
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PROGRESSION OF SMALLPOX
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• Incubation Period
• Pre-eruptive Stage • Macules • Papules • Vesicles • Pustules • Scabs • Scars |
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SMALLPOX CASE FATALITY* BY CASE TYPE & VACCINATION STATUS
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• The vaccine may prevent or ameliorate illness if given within 3 or 4 days of exposure.
• Passive immunization in the form of vaccinia immune globulin is most effective when administered in the first 24 hours after exposure. • The vaccine is not benign. At least one death per 1 million can be expected, as well as serious complications including secondary autoinoculations, generalized vaccinia infection, eczema vaccinatum, and post-vaccine encephalitis. |
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Togaviruses
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• two groups; Alphaviruses and Flaviviruses.
• enveloped and contain a positive stranded RNA genome. This group of viruses are called "arboviruses" because their life cycle involves alternating between vertebrates and arthropod vectors, mostly mosquitoes. • The Togavirus' natural cycle usually involves birds and mammals and rarely humans with the exception of those responsible for yellow fever and dengue fever. |
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Alphaviruses
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• Eastern and Western Equine Encephalitis (EEE, WEE): Following the bite of an infected mosquito, the resultant viremia is often asymptomatic. However, if the virus invades neural tissue, encephalitis may
result. This condition is marked by high fever, delirium, coma and possibly death due to convulsions and paralysis. • Venezuelan Equine Encephalitis (VEE): Similar to EEE and WEE, VEE has more systemic manifestations with less neural involvement. |
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WN viral encephalitis
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• While human infections with neurotropic arboviruses are usually clinically unapparent, most clinically apparent infections are febrile illnesses associated with a wide range of neurologic manifestations. These range from mild aseptic meningitis to fulminant and fatal encephalitis.
• Symptoms may include headache, stiff neck, confusion or other mental status changes, nausea, or vomiting. Signs may include fever, meningismus, cranial nerve abnormalities, paresis or paralysis, sensory deficits, altered reflexes, abnormal movements, convulsions, and coma of varying severity. • Arboviral meningitis or encephalitis cannot be clinically distinguished from other central nervous system infections. |
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Transmission of the Rubella virus is via the respiratory route
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• Prior to the introduction of the vaccine, rubella was a common, mild disease with a rash. It was found
worldwide and mostly affected children. • Initial multiplication occurs in the respiratory tract. One week after infection, viremia occurs and this is later followed by the skin rash. • If the virus infects a woman during the first 3-4 months of pregnancy, it may infect the placenta or fetus, multiply in any fetal organ and cause damage or death of certain cell types. This congenital rubella syndrome affects the eyes, heart and brain. |
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Picornaviruses
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• Picornaviruses are small, nonenveloped viruses containing a single positive strand RNA genome. They
possess an icosahedral symmetry. • Picornaviruses are divided into two groups; the Enteroviruses (Poliovirus, Coxsackievirus and Echovirus) and the Rhinoviruses. There are about 63 serotypes of Enterovirus and more than 100 serotypes of Rhinovirus. • Viruses linked to the common cold could be causing memory loss and Alzheimer's disease in millions of people, new research suggests. • Experts suspect that common viruses which infect around one billion people worldwide each year may be invading the central nervous system and damaging the brain. In later life this could lead to symptoms of memory loss and declining mental ability. |
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Polioviruses
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• Poliovirus types 1, 2 and 3 are recognized. Their genome contains a 7000 base positive strand of RNA. These viruses adsorb only to intestinal epithelial cells and motor neuron cells of the central nervous system.
• A number of syndromes can be observed, most (90-95%) are subclinical. About 4-8% present with a mild fever, sore throat and headache. • Nonparalytic polio occurs in about 1% of cases while paralytic disease affects only 0.1%. Of the paralytic conditions, about 5-10% affect the cranial nerve or medulla while the others are spinal and limited to muscle weakness rather than complete paralysis. |
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Coxsackie
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These viruses are divided into two groups; A and B. There are 23 serotypes of A, 6 serotypes of B. In humans, Coxsackieviruses produce respiratory disease, herpangitis, "hand, foot and mouth" disease, febrile rashes, pleurodynia, pericarditis, myocarditis, aseptic meningitis and paralytic disease.
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Echoviruses
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produce respiratory disease febrile illness (with or without a rash), aseptic meningitis
and paralytic disease |
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Rhinoviruses
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This group of viruses are sensitive to acid pH and their optimal growth occurs at 33°.
There are over 100 serotypes of Rhinoviruses and they produce the common cold |
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Orthomyxoviruses
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• The disease caused by these viruses, influenza, is an acute respiratory disease with prominent systemic
symptoms despite the fact that the infection rarely extends beyond the respiratory tract mucosa. • Type A is responsible for periodic worldwide epidemics; types A and B cause regional epidemics during the winter. • Influenza epidemics have been documented since 1173 AD; a pandemic in 1918 was responsible for 20 million deaths worldwide. |
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Influenza virus
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• Orthomyxoviruses contain a single stranded, negative RNA genome divided into 8 segments.
• The viruses have a lipid bilayer envelope with surface glycoproteins (hemagglutinin and neuraminidase) • There are 3 viral antigens of importance: the nucleoprotein antigen that determines the virus type (A, B or C), the hemagglutinin (H) antigen, and the neuraminidase (N) antigen. The H and N antigens are variable. • Viral attachment is mediated by the hemagglutinin. The virus enters host cells by pinocytosis and uncoating occurs by fusion of the viral envelope with the membrane of the vacuole. The RNA is capped and replication proceeds in the nucleus. The progeny are released by budding and cell death ensues. • The segmented genome of the influenza virus allows rearrangements to occur in simultaneously infected cells. This accounts for the periodic appearance of new variants. The new variants are responsible for the process of antigenic shift. This occurs every winter. • Pandemics result from rearrangement of the viral genome segments i.e., Antigenic shift. • Minor changes are called antigenic drift and these are responsible for many epidemics. They result from mutation in the viral RNA. • Antigenic drift occurs every 2-3 years while antigenic shift which cause pandemics occur every 10 years. • Changes in H and N |
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PATHOGENESIS of influenza
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• Transmission of disease is airborne. The viruses deposit in lower respiratory tract, their primary site is
the tracheobronchial mucosa. • Neuraminidase produces liquefaction, which leads to viral spread. • Respiratory symptoms include a cough, sore throat and nasal discharge. There is no viremia but systemic symptoms such as fever and muscle aches do occur. • The extent of respiratory tract cell destruction is a probable factor in the disease. Severe complications include pneumonia (viral or bacterial). |
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Mumps, Measles, Respiratory Syncytial Virus
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• an important cause of respiratory disease in children. Illnesses include croup, bronchiolitis and pneumonitis.
• This group of viruses share similar features; they possess a double layered envelope with spikes, have a helical symmetry and contain a negative stranded RNA genome. An RNA-dependent RNA polymerase (RDRP) is contained within the virus particle. |
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Rubella virus: measles
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• Produces the disease commonly known as German measles. Severe manifestations when affecting a pregnant woman during the first trimester because of the potential for birth defects
• measles is perhaps best known for its rash, it is really a respiratory infection. The first symptoms are irritability, runny nose, eyes that are red and sensitive to light, hacking cough, and a fever (temperature as high as 105°F). • One possible identifying sign of measles is Koplik's spots. These are small, red irregularly shaped spots with blue-white centers found inside the mouth. |
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RSV: Respiratory Syncytial virus
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• a major cause of bronchiolitis and pneumonia in infants under 1 year. Reinfection in adults usually involves the upper respiratory tract. The viruses produce a characteristic syncytia formation, hence the name. There is only one serotype that affects humans.
• Respiratory Syncytial Virus (RSV) is the most common cause of respiratory illness and a major cause of morbidity in children |
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Parainfluenza
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About 30-40% of acute respiratory infections in infants and children can be attributed to the Parainfluenza virus. Disease ranges from mild and cold-like to lifethreatening (croup, bronchiolitis and pneumonia). Parainfluenza viruses are the most common cause of croup
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Mumps
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• A common acute disease of children, the mumps virus produces inflammation of salivary glands leading
to obvious enlargement. • This girl has mumps, a disease that is not commonly seen anymore because of vaccination. • Paromyxoviruses are the most common cause, although other viruses can cause this disorder. • Bilateral parotid duct swelling is common and usually occurs in the age 5 to 15 year range. Orchitis can occur when men are infected, with occasional sterility as a result. • Outbreak in midwest in sp 2006 - ~2000 college students |
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Rhabdovirus: Rabies
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• Rhabdoviruses generally enter via a bite or a wound infected with saliva.
• virus replicates at the site and then infects central nervous system (CNS) tissue. Following a variable (6 days up to 1 year, average 30-70 days) incubation period, the virus spreads rapidly via the nerves. CNS damage produces the symptoms of disease. • Neurons accumulate ribonucleoprotein as intracytoplasmic inclusions (Negri bodies). Infection of the thalamus, hypothalamus or pons may occur. • Symptoms include fever, excitation, dilation of the pupils, excessive lacrimation, salivation, anxiety, hydrophobia due to spasms of the throat muscles and, eventually, death. |
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Retroviruses
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• Oncornaviruses: HTLV 1, HTLV 2, HTLV 5
• Lentiviruses: HIV 1, HIV 2 • The HTLV or Human T Cell Lymphotrophic Viruses are divided into three types based on the type of diseases they produce: – HTLV-I produces cutaneous T-cell lymphomas, – HTLV-II produces hairy T-cell leukemias, – HTLV-V produces T-cell lymphomas and leukemias. • The Retroviruses are RNA viruses and their name is derived from the viral enzyme Reverse Transcriptase, which makes circular DNA from linear RNA. The viral DNA has the capacity to integrate into the host cell genome. – HIV-1 produces Acquired Immunodeficiency Syndrome (AIDS), – HIV-2 produces a related disease syndrome, restricted to W. Africa. • In general, the viruses are not cytopathic. The Oncornaviruses generally transform cells, causing leukemias, sarcomas and carcinomas. • The Lentiviruses attack T-cells, all but abolishing the host immune response. * The U.S. Food and Drug Administration (FDA) has approved a number of drugs for treating HIV infection. * • The first group of drugs used to treat HIV infection, called nucleoside reverse transcriptase (RT) inhibitors, interrupts an early stage of the virus making copies of itself. • Included in this class of drugs (called nucleoside analogs) are AZT, ddC (zalcitabine), ddI (dideoxyinosine), d4T (stavudine), 3TC (lamivudine), abacavir (ziagen), and tenofovir (viread). • These drugs may slow the spread of HIV in the body and delay the start of opportunistic infections. |
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Treatment
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More recently, FDA has approved a second class of drugs for treating HIV infection. These drugs, called protease inhibitors, interrupt virus replication at a later step in its life cycle. They include
» Ritonavir (Norvir) » Saquinivir (Invirase) » Indinavir (Crixivan) » Amprenivir (Agenerase) » Nelfinavir (Viracept) » Lopinavir (Kaletra) |
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Viruses
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must have a piece of DNA or Rna w/a protien code, & must have a living cell in order to replicate
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virus growth cylce
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1. attachment
2. endocytosis 3. penetration 4. uncoating |
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HPV growth cylce
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1/ Virion attaches to host cell
2. Virion penetrates cell and its DNA is uncoated 3. Early transcription and translation; enzymes are synthesized 4. Late transcription; DNA is replicated 5.Late translation; capsid proteins are synthesized 6. Virions mature 7. Virions are released |
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Viruses Growth Cylce
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1. ATTACHMENT phage attaches to host cell
2. PENETRATION phage penetrates host cell and injects its DNA 3.BIOSYNTHESIS phage DNA directs synthesis of viral components by the host cell 4. MATURATION viral components are assembled into virions 5. RELEASE host cell lyses and new virions are released |
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Viruses- lytic cycle
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1. Phag attaches to host cell and injects DNA
2. Phage DNA circulates and enters lytic cycle 3. New phage DNA and protiens are synthesized and assembled into virions 4. Cell lyses, releasing phage virions |
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Viruses- Lysogenic cycle
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1. Phag attaches to host cell and injects DNA
2. Phage DNA circulates and enters lysogenic cycle 3. Phage DNA integrates within the bacterial chromosome by recombination, becoming a prophage 4. Lysogenic bacterium reproduces normally 5. Occasionally, the prohpage may excise from the bacterial chromosome by another recombination event, initiating a lytic cycle |
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growing viruses
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1. a tissue is treated w/enzymes to separate the cells.
2. cells are suspended in culture medium 3. Normal cells or primary cells grow in a monolayer across the glass or plastic container. Transformed cells or continuouse cell cultures do not grow in a monolayer |
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DNA enveloped
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- herpesvirus
- poxvirus - hepatitis B |
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DNA nonenveloped
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- Papovavirus
- Adenovirus |
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RNA positive strand polarity enveloped
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- Togavirus
- Rubellavirus - Retrovirus |
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RNA positive strand polarity nonenveloped
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- Picomavirus
- Hepatitis A. |
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RNA negative strand polarity enveloped
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- Orthomyxovirus
- Paramyxovirus - Rhabdovirus |
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STD from highest to lowest
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1. Herpes (45 mil)
2. HPV ( 20 mil) 3. Chlamydia (2 mil) 4. HIV (560,000) |
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HIV replication
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1. Retrovirus penetrates host cell
2. After uncoating, reverse transcription of the viral RNA produces double-stranded DNA 3. The new viral DNA is transported into the host cell's nucleus and integrated as a provirus. The provirus may divide indefinitely with the host cell DNA 4. Transcription of the provirus may also occur, producing RNA for new retrovirus genomes and RNA that codes for the retrovirus capsid and envelope proteins. 5. Mature retrovirus leaves host cell, acquiring an envelope as it buds out |
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HIV replication
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1. Attachment
2. Uncoating 3. Reverse Transcription 4. Integratin 5. Proviral Transcription 6. Translation 7. Cleavage 8. Assembly, Maturation, & Release |
