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197 Cards in this Set
- Front
- Back
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what are viruses? |
acellular, obligate intracellular parasites infecting EVERY type of cell
-nonliving -lack metabolic system |
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Name characteristics of viruses |
1. obligate intracellular parasites of living cells 2. lack metabolic system (contain no ADP or ATP, FAA, sugars) and lack enzymes and machinery (ribosomes) for protein synth 3. take control of host cells processes 4. infect limited # of cell types 5. protected from much of host's immune response 6. contain either DNA or RNA |
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Can you see viruses? |
with an electron microscope
-animal viruses range from 22 nm (yellow fever) to 110 (HIV) to 450 (mimivirus but don't infect humans) * poxvirus is the largest human infecting virus
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Why are there new viruses? |
globalization |
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How are viruses different than other pathogens? |
1. acellular 2. reproduce via assembly 3. all viruses are haploid (except retrovirus) 4. viruses contain DNA or RNA not both (except cytomegalo virus 5. lack organelles, cytoplasm, nucleus, nucleoid |
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What do viruses look like? |
genome surrounded by outer protein coat (capsid) which can be surrounded by envelope made of lipid membrane from host cell.
13 of 19 families of animal viruses are enveloped *must remain wet and are transmitted via fluids (don't survive harsh GI tract) |
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genome is surrounded by capsid made up of: |
-identical protein subunits called capsomers - self assemble into capsid -2 symmetrical structures: helical and icosahedral |
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What is the appearance of a helical virus? |
1. naked helical viruses are rigid and tightly wound into a cylinder ( if enveloped, it will be looser) |
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What is the appearance of an icosahedral virus? |
20 triangular faces and 12 corners (some have 1 type of capsomer while others havee different types) |
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What is the function of viral capsid/envelope? |
1. protect virus core which contains genome 2. recognize host cells and bind to them 3. help introduce viral DNA/RNA into suitable host cell 4. stimulate immune system to produce ABs that protect against future infections |
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combination of capsid and genome is: |
nucleocapsid |
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What is the genome? |
DNA or RNA....DNA viral genomes are ss linear, ds linear or ds circular - RNA genomes are ss linear, ss linear negative and segmented, ss circular negative-sense or ds linear and segmented |
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Exceptions to DNA/RNA rule: |
parvovirus = ssDNA reovirus= dsRNA |
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What is a mutation? |
change in nucleotides within a single genome |
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Influenza is what kind of genome? |
segmented |
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What is a strain? |
same virus but isolated from different patient or geographical locations
*H1N1: resistant to Tamiflu but sensitive to Relenza |
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What is a type? |
same virus but RESPONDING differently to antibody detection
*serotypes *adenovirus causing conjunctivitis in humans (51/100 serotypes) |
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What is a variant? |
virus whose phenotype differs from wild type (genetic mutation is not known)
* HIV variants resistant to RT inhibitors |
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What is the rate of mutations in DNA virus? |
1x10^-9 |
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What is the rate of mutation in animal cells? |
1x 10^-9 |
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What is the rate of mutation in RNA viruses? |
1 in 1000.
bc of RNA dependent RNA polymerases with more error prone (no proofreading done here) |
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What is the only RNA virus that doesn't encode a RNA dependent RNA polymerase? |
reverse transcriptase....it contains an RNA dependent DNA polymerase *poor fidelity and proclivity...no proofreading .
*error rate= 1 per cycle |
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Recombination is ... |
genetic information exchanged between two distinct genomes
-2 mechanisms: 1. strand breakage and religation= occurs with all viruses that use a DNA intermediate 2. copy choice occurs only in RNA viruses; viral polymerase switches template strands during replication |
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What is reassortment? |
exchange of genetic material between two segmented genomes....only RNA can do this
*influenza A virus |
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What are the steps of viral replication? |
1. recognition of host cell 2. attachment 3. penetration 4. uncoating 5. synthesis of nucleic acids/proteins 6. assembly 7. release from host cell |
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What is attachment? |
specific binding of viral protein to cellular protein....attachment protein is usually glycoprotein id it is enveloped or a surface peptide if the virus is naked..... |
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What is tropism? |
interaction of a viral attachment protein with a cellular receptor protein. specificity for a certain cell type
*hepatitis A has a tropism for HEPATOCYTES |
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Explain attachment of a naked virus |
interaction between viral capsid proteins and host cell receptor (example: rhinovirus's ligand too small for antibody to get in and bind. avoids being recognized by the immune system |
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Explain the attachment of an enveloped virus |
viral envelope has spikes that protrude and will interact with host cell receptor |
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What are the three ways penetration can be accomplished? |
1. direct penetration 2. fusion 3. endocytosis |
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What is direct penetration? |
-only seen in named viruses ... only genetic material enters while capsid stays outside |
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what is fusion? |
-only seen with enveloped viruses...viral envelope contains many host cell proteins so this will merge and become part of membrane......both capsid and genome enter host cell |
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What is endocytosis? |
internalization of clathrin coated or cave-in coat pits at the cell membrane.....once attached, both enveloped or naked viruses may be endocytosed |
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What is uncoating? |
removal of capsid to expose viral genome to the inside of the host cell....allows subsequent expression and replication of the viral genome |
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Once uncoated, what does RNA viruses commonly do? What is the exception? |
remain in the cell cytosol for replication and gene expression....retrovirus is exception (uses DNA in nucleus) |
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Once uncoated, what does DNA viruses commonly do? What is the exception? |
it is transported to nucleus (exception is pox virus...brings own enzymes as it is huge and is able to replicate in the cytoplasm) |
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What advantage do +RNA viruses have? |
RNA can be used directly as mRNA.....in any other case mRNA must be synthesized. |
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If you have +- dsDNA, how do you get +mRNA? |
transcribe - strand of dsDNA |
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If you have + ssDNA, how do I get mRNA? |
synthesis of - strand.....make +-dsDNA....transcribe -strand |
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If I have +ssRNA but reverse transcriptase, how do i get +mRNA? |
RT makes DNA from ssRNA.....-ssDNA will use replicase to copy -strand....+-dsDNA intermediate.....transcribe - strand to make +mRNA |
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If I have +-dsRNA, how do i get mRNA? |
transcribe the - strand |
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If i have -ssRNA, how do i get mRNA? |
transcribe the - strand |
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If i have +ssRNA, how do i get mRNA? |
you can directly use it as mRNA |
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What is protein synthesis? |
once mRNA is made, and genetic material has entered the nucleus for replication, mRNA will be produced there also and will exit nucleus for translation |
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What is DNA genomic synthesis? |
replicated via direct DNA to DNA copying either by viral or cellular DNA polymerase enzymes.
*dsDNA usually replicate int he nucleus (except poxvirus *ssDNA viruses replicate in nucleus via dsDNA intermediate |
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What is RNA genomic synthesis? |
non retrovirus RNA genomes are replicated from RNA to RNA via viral replicase enzyme (RNA dep RNA polymerase) |
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Before assembly what must a virion contain? |
1. viral nucleic acid 2. accessory proteins 3. viral enzymes required for infection in the next cell |
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What is assembly? |
as genes are expressed and translation occurs, viral particles are concentrated in host cell, they will work together to form a larger structure |
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What are inclusion bodies? |
compact masses of viruses that may be present in nucleus or cytoplasm |
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How are icosahedral capsomers assembled? |
spontaneously and genome includes a packaging sequence which is bound by a protein that stuffs the genome into the capsid |
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How are helical capsomers assembled? |
uses genomic material as starting point which have a pac sitewhere the capsomer subunits bind to begin the process of assembly. continue until completely surrounded |
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What is maturation? |
changes to make it better suited...common change= processing of protein precursors into their final products through protease activity
*if not made, it will not be infectious |
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What are the three mechanisms of release? |
1. budding 2. cell lysis 3. endocytosis |
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What is budding? |
only in enveloped viruses....assembled visions distend through embrace and becomes enveloped....can take place via plasma membrane (HIV), nuclear membrane (herpes), endoplasmic reticulum (Hep B), or vesicles (influenza) |
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What is cell lysis? |
direct result of virus replication or when overwhelmed by viral load....when cell dies, breaks open and releases viral particles. only naked viruses |
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What is exocytosis? |
similar to budding but not acquiring portion of cell membrane |
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True or False: Cell must be permissive of virus in order for infection to occur? |
True. |
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What are the different types of viral infections? |
1. abortive (failed infection) 2. lytic (cell death) 3. persistent (no cell death)--this breaks into 4 other parts |
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What are the 4 types of persistent viral infections? |
1. chronic 2. latent 3. recurrent 4. transforming |
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What are abortive infections? |
mature visions are not produces; virions can enter cell but doesn't proceed all of the replication steps. may require confection with helper virus to mature |
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What are acute/lytic infections? |
rapid onset period of dz followed by clearance of virus....often resultt in cell death |
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What are persistent infections? |
linger and not readily cleared by immune system. host cell survives and horrors virus |
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What are chronic infection and name an example |
can be lifelong; continuous production and shedding of virions
**Hepatitis B and C in liver |
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What are latent infection? Name examples. |
intermittent periods of viral replication and shedding with LONG periods of dormancy when the virus is not replicating.
**Herpes simplex and varicella- zoster (chicken pox) in neurons and activated after stress, injury, exposure to UV light, or during period of immune suppresion (during AIDS or organ transplantation) |
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What are transforming infections? |
virus causes cell to lose growth control via over expression of growth factors. can lead to tumor formation **HTLV |
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What is the name of damage caused by viruses on host cells? |
cytopathic effect...accumulated damage that alters microscopic appearance of host cell (size, shape, inclusion bodies) |
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What are examples of oncogenic viruses? |
HPV and HTLV I and II |
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What are the steps of viruses causing disease? |
think "EIESCS"
1. Entry into host 2. immune evasion 3. entry into cells and primary replication 4. spread within host 5. cell injury and clinical illness 6. shedding of new virions |
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How do most viruses enter host? |
mucosal surface (90% of our body covered with this type of tissue)...sometimes via breaks in skin or needle/bite |
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What is localized infections? |
occurs at the site where virus entered host
**ex: rhinitis, rotavirus |
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What are generalized infections? |
spread beyond point of entry to specific tissues for away (hepatitis) or systemic (measles) |
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Entry through respiratory tract.... |
most common point of entry via visions in aerosol (sneeze) or saliva exchange....
---what protects us? ciliated cells, mucus, alveolar macrophages and specific ones (IgA) |
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Entry through alimentary tract.... |
acid, bile, proteolytic enzymes inactivate many viruses but some become resistant.... |
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Which viruses infect the GI tract? |
naked!
---since bile easily disrupts lipid bilayers on enveloped viruses (need fluid environment) |
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Why is the esophagus rarely infected? |
1. swallowing mechanism 2. tough lining |
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What viruses enter through abrasions in the skin? |
1. herpes simplex virus 2. poxvirus |
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Examples of diseases transmitted via bite |
1. west nile 2. malaria |
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Sharing of needles can transmit viruses in bloodstream like: |
1. hep B and C 2. retroviruses (HIV, HTLV) 3. cytomegalovirus 4. Epstein-Barr virus 5. ebola |
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Genital tract entry |
herpes simplex and papillomaviruses are localized; HIT, HTLV and Hepatitis are STDs and generalized |
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Conjunctiva entry |
less resistant than skin and prevents infection via production of tears and blinking!
*can enter via injury, ophthalmic procedures, unsanitary liquids (pool water) |
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What are some immune evasion mechanisms? |
1. inhibiting antigen presentation by host cell 2. antigenic variation 3. molecular mimicry 4. priviliged sites |
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How do viruses inhibit antigen presentation? |
downregulating expression of MHC class I molecules so host cell can't present viral antigens to T cells to activate immune response |
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What is antigenic variation? |
change/remove surface proteins so antibodies will no longer recognize virus |
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What is molecular mimicry? |
express a surface protein similar to host protein |
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What is a privileged site? |
enter immunologically advantageous anatomical location with little immune protection (eye, brain, testes, ovary) |
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What is local spread of virus? |
1. local speed on epithelial surfaces (mucus/ fluid movement in respiratory allows flu virus to spread to epithelial cells nearby....short incubation time) vs. papillomavirus that infect basal later of epidermis and mature as keratinization...long incubation time |
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What is sub epithelial invasion and lymphatic spread? |
if it enters lymphatic capillary it can reach lymph node where it is engulfed by macrophage or goes into bloodstream
ex: rabies virus (muscle--nerves--SC--CNS) |
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What is viremia? |
presence of virus in bloodstream ***most effective vehicle for spread of the virus
1. primary viremia= transfer virus to specific organ 2. secondary viremia- after |
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What viruses can cross placenta? |
B19, rubella CMV |
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What viruses can occur perinatally in birth canal? |
herpes simplex |
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Parvovirus and viral can cause...... |
fetal death and abortion |
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Cytomegalovirus and rubella cause |
congenital defects |
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HIV can be transmitted from mother to infant via? |
1. in utero 2. during birth process 3. breast feeding**most common |
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What are TORCH organisms? |
group causing symptomatic birth defects in newborns...blood test measuring presence of antibodies for these organisms |
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T in Torch= |
toxoplasma |
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O in TORCH? |
other (syphilis, HBV, coxsackie virus, EBV, VSV, human parvovirus) |
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R in TORCH? |
rubella |
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C in TORCH |
cytomegalovirus |
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H in TORCH |
herpes Simplex virus |
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What is virulence? |
relative capacity of a pathogen to infect and harm the host cell |
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What is shedding? |
release of virus into the environment |
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How is viral pneumonia's site of entry synonymous with site of shedding? |
viral infection in Resp tract; shed via coughing into the air (sneezing = 20000 droplets and coughing is hundreds)
**another example is herpes in dorsal root ganglia |
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In generalized diseases, like poliovirus, how is this shed? |
enter through alimentary tract, spread thru blood, axons and peripheral nerves
shed in stools and present before onset of illness
**HIV shed through body fluids |
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How can you diagnose a viral infection? |
clinical symptoms, time of year, travel history, lab diagnosis |
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How is collecting appropriate sample critical? |
depends on type of infection; stored at 4-8 degrees if processed in days.....-70 if much later date |
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You should exam for what effects to diagnose |
cytopathic effects |
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What are the four methods to diagnose viral infections? |
1. direct examination 2. serological methods 3. molecular methods 4. virus cultivation |
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What is direct examination? |
microscopic examination of tissues or cells can reveal CPE to the cell and in most cases they need to be confirmed |
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what kind of microscopy can detect individual viral particles? |
electron microscopy; fecal and vesicular samples common (not respiratory) |
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What do serological methods help with? |
utilize specificity and sensitivity of antigen-antibody interactions ( examples: ELISA, direct assays= detect viral antigens or indirect assays= detect antiviral antibodies) |
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What is immunoflourescence microscopy? |
combine LIGHT MICROSCOPY with SEROLOGY by utilizing fluorescent tags attached to antibodies to detect present of antigens or antiviral antibodies |
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What are immunoassays? |
highly sensitive and detect as little as 1 ng of viral antigen per milliliter of ample |
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EIA |
enzyme linked immunosorbent assay (ELISA). 2 antibodies used: primary antibody (bind to antigen) and secondary (binds to Fc region of primary antibody)........enzyme is linked to secondary antibody and causes color change when appropriate substrate is added and cleaved by enzyme |
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What is western blot? |
proteins extracted from a sample and separated in acylamide gel via electrophoresis then transferred to solid membrane and washed with Enzyme-linked antibodies....when substrate added, color develps.
**this identifies presence and size of specific viral proteins |
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What are two molecular methods used to diagnose viral infections? |
1. PCR 2. nucleic acid hybridizations |
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What is pCR? |
minute amounts of DNA needed, doesn't require isolation of the infectious agent, once large quantities made, can be sequenced to identify agent
**15-25 oligomers used to amplify |
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What is nucleic acid hybridizations? |
viral nucleic acids detected in patients blood or tissues with complementary DNA or RNA. complementary proves are linked to a radioactive label and samples are exposed to film to determine if hybridization happened. |
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What other techniques use basic principles of nucleic acid hybridizations? |
Souther blots, Northern blots; dot blot hybridizations; in situ hybridization |
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What is Southern Blot? |
identify DNA extracted from tissue samples and separated by electrophoresis
**northern blot test for presence of RNA |
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What is dot blot hybridizations? |
nucleic acids are extracted from tissues and spotted onto a nitrocellulose membrane to which the labeled probe is added and allowed to bind |
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What is in situ hybridization |
allows ID and location of viral nucleic acids inside the host cells |
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How are viruses cultivated? |
1. live animal 2. bird embryos 3. tissue culture |
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explain live animal inoculation |
virus injeceed into brain, blood, muscle, body cavity, skin, footpad of animal.. |
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explain bird embryo inoculation |
undergo embryonic development within confines of egg(fluff nutrition)....signs of growth= death, defective developlment, localized damage in opaque spots (pocks) |
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Explain tissue/cell culture techniques |
animal cell cultures grown in sterile chambers and grow as a mono layer.....primary cell cultures prepared from isolated animal tissue (embryonic, fetal, adult, cancer)....they don't grow indefiniitely.
**takes long to accomplish |
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How to keep track of virus? |
1. classify by: host infected, structure of virus, similarities in genetic makeup...
**classification sequence is order-family-genus-species (virales-viridae--virus-virus) |
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What are the 6 approaches to prevent and control viral disease? |
QHVCIA 1. Quarantine 2. Hygiene and sanitation 3. Vector control 4. change of lifestyle 5. immunization 6. antiviral chemotherapy
*bold means community |
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What does quarantine do? |
WHO used against smallbox but not practical becausee of travel.....ensure proper hygiene and sanitation |
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Describe vector control |
mosquito control is an example....WHO limits their populations by destroying the breeding sites |
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Describe lifestyle changes examples |
reduce sharing of needles and sexual responsiblity |
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Describe immunization |
divided into 2 parts...active (natural exposure or artificial) and passive (breast feeding) |
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What is passive immunity? |
administration of pre made antibody as short term protection or emergency (venom)**hepatitis B, babies born to mothers with chicken pox, persons bitten with potentially rabid animal)
**mothers provide passive immunity to newborns through Ig in milk or serum |
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What are three important antiviral Ig preparations |
1. HBIg (hepatitis B) 2. VZIg (varicella zoster) 3. RIg (rabies) |
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What is active immunization? |
induction of an immune response by administration of antigen (vaccine)...prevent spread of a viral disease inside a host (herd immunity) |
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To be a successful antiviral agent, the rug must: |
1. target viral function/structure that is unique 2. must interfere with a cellular function so that the virus cannot replicate 3. must kill only virus-infected cells |
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What are the limitations to antivirals? |
1. difficult to target only virus-specific processes or structures 2. drugs may be ineffective if too many virions have been produced by the time drugs are given 3. virus becomes latent 4. emergence of drug resistant strains |
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What drugs are nucleoside analogs? |
acyclovir, valacyclovir, famiciclovir, penciclovir, ganciclovir, ribavarin |
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What drugs are nucleotide analogs? |
cidofocvir, adefovir |
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What drugs are non nucleoside reverse transcriptase inhibirots? |
delavirdine, efavirenz, etravirine, nevirapine |
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What drugs are antisense drugs? |
formivirsen |
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What drugs are topical immune modulator? |
imiquimod |
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What drugs are INF-alpha or in combo? |
inf-a, peg inf a, ribavirin |
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which are ion channel function inhibitors or neuraminidase inhibitors? |
amantadine, rimantadine, zanamivir, oseltamivir |
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Which are pyrimidines? |
trifluridine |
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Which drug is a synthetic acyclic analog of Guanosine and acts agains HSV (DNA viruses? |
acyclovir |
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What is the mode of action for acyclovir? |
monophosphate is phosphorylated to triphosphate via thymidine kinase and can now integrate itself into viral DNA and inhibits DNA replication |
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What is the drug theat the FDA approved as a buccal tablet in April 2013? |
Sitavig (acyclovir) |
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What is the drug that is used for the post exposure prophylaxis of varicella zoster and is via immunoglobins? |
VariZIG |
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What is the L-valine ester of acyclovir? |
Valacyclovir |
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What is the mode of action for valacyclovir? |
converted to acyclovir and runs its course. |
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What is the advantage for valacyclovir?Disadvantage? |
1. less doses req'd and higher plasma concentration attained 2. no IV form is available
**dont use with patients that have hemolytic uremic syndrome |
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What drug is rapidly phosphorylated by thymidine kinase to penciclovir monophosphate? |
famciclovir
*penciclovir will inhibit viral DNA polymerase |
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What is Foscarnet? |
synthetic pyrophosphate analog....directly inhibits viral enzymes without incorporating into viral DNA
**drug of choice when acyclovir resistant |
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What is the mode of action for Foscarnet? |
binds to DNA polymerase and prevents cleaving pyrophosphate from newly added deoxynucleoside triphosphate-----DNA chain is halted.
**also, inhibits HIV-1 reverse transcriptase |
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What is Trifluridine/Viroptic? |
fluorinated pyrimidine nucleoside; results in non-functional viral proteins |
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What drug prevents viral entry? |
n-docosanol /Abreva
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What drug is a synthetic purine nucleoside analog and is used to treat CMV? |
ganciclovir |
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What is the mode of action for ganciclovir? |
ganciclovir monophosphate phosphorylated--integrate into viral DNA which inhibits viral DNA polymerase..penetrates infected and non infected cells |
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What is the L-ester of ganciclovir |
Valganciclovir *converted in vivo to ganciclovir |
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What is cidofovir? |
synthetic acyclic purine nucleotide *inhibits viral DNA synthesis via diphosphate form *treat CMV infections in AIDS patients
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What drug is used against HPV and molluscum contagiousom (member of poxvirus)? |
cidofovir |
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What drug is the first anti-sense drug to be FDA approved? |
Fomivirsen/Vitravene *ss antisenseDNA complementary to CMV mRNA and inhibits protein synthesis **may not be able to impart resistance |
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What are topical immune modulators? |
act non-specifically |
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What is the drug that induces cytokines and stimulated IL-1, IL-6, IL-8, TNF and INF-alpha? |
Imiquimod.....affects both acquired and innate immune mechanisms |
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What is INF? |
glycoprotein produced by fibroblasts and WBC in response to stimuli....have antiviral and anticancer properties
good alternative to artificial antiviral agents |
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What is INF-alpha? |
binds specifically to membrane receptors on cell's surface...results in inhibition of viral replication
**result in augmentation of macrophage phagocytic activity and lymphocyte cytotoxicity |
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What drug is the only one used for viral infections? |
INF-alpha |
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What is PEG-INF? |
increases half life of INF, better efficacy, less serious side effects.....in combo with ribavirin, it is most effective in treating HCV viruses |
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What is Ribavirin? |
synthetic nucleoside analog used to treat respiratory syncytial virus (RSV) infections |
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What is the mode of action for ribavirin? |
--prevents nucleic acid synthesis *active against RSV, influenza A and B and HSV |
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What is the primary toxicity of ribavirin? |
hemolytic anemia |
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What is the problem with ribavirin? |
highly carcinogenic effects to fetus via inhalation
***INF alpha + ribavirin is more effective than taking each individually |
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What is a synthetic tricyclic amine that is effective against influenza A? |
amantadine/symmetrel |
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What is the mode of action of amantadine/symmetrel? |
interferes with the ion channel function of the M2 protein and acts indirectly on hemagglutinin the viral protein which facilitates viral adsorption and entry. |
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Which influenza lacks M2 protein? |
Influenza B |
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What is Rimantidine/Flumadine? |
alpha methyl derivative of amantadine effective on influenza A |
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What is the mode of action of rimantadine? |
inhibition occurs early during viral replication and might possibly affect viral uncoating |
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What is Zanamivir (Relenza)? |
neuraminidase inhibitor, FDA approved to treat uncomplicated Flu A and B for ages 7 and older (orally)
**increased risk of skeletal birth defects when given in high doses to pregnant |
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What is the mode of action for zanamivir? |
inhibits viral neuraminidase and prevents replication of influenza A and B |
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What is the drug that is pharmacologically similar to Zanamivir but structurally different |
Oseltamivir (Tamiflu)
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Wht is the mode of action for Tamiflu? |
prodrug that is hydrolyzed to oseltamivir carboxylate in vivo and inhibits viral neuraminidase and prevents replication of influenza A and B |
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What is Victrelis (Boceprevir)? |
treatment for chronic HepC....inhibitor of HepC virus non structural protein 3 (NS3) serine protease
**used for people with cirrhosis too |
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What drug is a hepC NS3/4A protease inhibitor? |
Incivek
*has a boxed warning for fatal skin rxns |
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What is Olysio (Simeprevir)? |
protease inhibitor for HepC that showed reduced effectiveness in patients with genotype 1a hepC with NS3 Q80K polymorphism |
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What is Sovaldi (Sofosbuvir)? |
nucleotide analog inhibitor that blocks hepC virus replication *without need for co-administration of interferon *demonstrated efficacy in participants who could not tolerate interferon |
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FDA approves first combo pill to treat HepC on October 10, 2014. What drugs? |
Harvoni (ledipasvir and sofosbuvir) to nail the genotype 1 infection and doesn't require interferon |
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What is the current standard of care in the US for HepC? |
take ribavirin plus Sovaldi or Olysio + PEG-INF |
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What is a fusion inhibitor? |
(enfuvirtide/Fuzeon): binds to GP41
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What is Maraviroc/Selzentry? |
blocks CCR5 to prevent entry of virus into macrophages; CCR5 co receptor antagonist and first drug approved in new class of anti-HIV meds |
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What are protease inhibitors? |
*inhibit maturation steps of HIV by targeting apartyl protease enzyme which is important for cleaving the gag-pol polyprotein into individual proteins required for infectivity **Made AIDS manageable |
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What are integrase inhibitors? |
raltegravir/Isentress; RAL
**blocks action of integrates that aids in integrating viral geneticc info into the genome of the target cell ( only approved for salvage therapy) |
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What drug used to treat HIV-1, integrase strand transfer inhibitor? |
Tivicay |
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What are entry inhibitors? |
CC5 co receptor antagonists that selectively bind to human cytokine receptor CCR5 present on the membrane of CD4 cells, preventing interaction of GP120 and CCR5 thus preventing entry into cells |
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What is the standard of care for anti-retroviral treatment? |
1 or 2 protease inhibitors in combo with 2 nucleoside RT inhibitors to block viral replication at different stages |
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What is a combination of EMTRIA and VIREAD that is used in combo with other antiretroviral agents to treat HIV1 infection? |
Truvada |
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What is Palivizumab (Synagis)? |
only antiviral monoclonal antibody treatment approved for respiratory syncytial virus infection (antibody is directed against viral surface glycoprotein F protein) |
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What is epidemiology? |
study of frequency and distribution of disease in defined human populations. |
