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Virology + Antiviral
Day 7
| Question | Answer |
|---|---|
| Which type of viral genetics is associated with worldwide influenza pandemics? | Reassortment (viruses with segmented genomes exchange segments) |
| In which type of viral genetics will the progeny revert back to the old virus because there is no genetic exchange (virus A only picks up nucleocapsid proteins from virus B) | Phenotypic mixing |
| Which vaccines are egg based and require a skin test for people with egg allergies prior to administration? | The flu and yellow fever (yellow like an egg yolk) |
| What is the ONLY live vaccine that may be given to HIV patients? | MMR (can only give to HIV; do NOT give to AIDS patients); besides MMR, live vaccines should NEVER be given to immunocompromised patients or their close contacts (herd immunity) |
| Which form of the influenza vaccine is live? | Intranasal form only (IM form is killed vaccine) |
| Which vaccines are live? | Smallpox, yellow fever, chickenpox (VZV), Sabin's polio, MMR Chickens are alive. Sabin (saber) tooth tigers are alive. |
| Which vaccines are killed? | Rabies, Influenza, salk Polio (k=killed), and hAv (RIP Always) |
| Which vaccines are recombinant? | HBV and HPV |
| What is the only single stranded DNA virus? | Parvoviridae (parvovirus B19) |
| What is the only double stranded RNA virus? | Reoviridae (Reovirus= Colorado tick fever, Rotavirus= diarrhea in children) |
| Where do DNA viruses replicate? | In the nucleus |
| Where do RNA viruses replicate? What are the exceptions to this rule? | In the cytoplasm; except for influenza and retroviruses |
| Most enveloped viruses acquire their envelopes from the plasma membrane when they exit the cell. Which virus is an exception to this rule? How does it acquire its envelope? | Herpesviruses; acquire envelopes from nuclear membrane |
| What are the DNA viruses? | Herpesviruses, HepaDNAvirus, Adenovirus (sounds like "A DNAvirus"), Parvovirus, Papillomavirus, Polyoma virus, and Pox virus (HHAPPPPY) |
| Sporadic temporal lobe encephalitis | HSV-1 |
| Virus assoc'd with t(8;14) | EBV (Burkitt's lymphoma= t(8;14) |
| Infection in immunocompromised patients, especially transplant patients | CMV |
| AIDS retinitis | CMV |
| Roseola | HHV6 |
| Kaposi's sarcoma | HHV8 |
| Positive monospot infectious mononucleosis | EBV |
| Negative monospot infectious mononucleosis | CMV (listeria and toxoplasma can also cause - monospot test) |
| Neonatal herpes | HSV2 |
| Cowdry Type A owl's eye inclusions | CMV |
| High fevers that break and are then followed by a rash; may cause seizures if child is susceptible to febrile seizures | Roseola (HHV6) |
| Remains latent in trigeminal ganglia | HSV1 (makes sense cuz it's on your face!) |
| Remains latent in sacral ganglia | HSV2 (makes sense cuz it's on your butt!) |
| Remains latent in trigeminal and dorsal root ganglia | VZV |
| Herpes virus that infects B cells | EBV (B for B cells! Woo hoo!) |
| Herpes virus that infects mononuclear cells | CMV |
| What does the Tzanck test look for? | Multinucleated giant cells in HSV identification |
| Fever, hepatosplenomegaly, exudative pharyngitis, and lymphadenopathy (esp posterior cervical nodes) | EBV |
| What does a positive monospot mean? | Heterophil antibodies are present |
| Assoc'd with nasopharyngeal CA | EBV |
| Not a retrovirus but has reverse transcriptase | Hep B |
| Febrile pharyngitis (w/acute hemorrhagic cystitis), pneumonia, and conjunctivitis; may be seen with GI problems | Adenovirus (DNA) |
| Aplastic crises in sickle cell disease | Parvovirus B19 |
| RBC destruction in fetus leading to hydrops fetalis | Parvovirus B19 |
| Anal cancer | Papillomavirus (16, 18) |
| Progressive multifocal leukoencephalopathy in HIV patients | JC virus (Polyomavirus; DNA) |
| Vaccinia | Cowpox (poxvirus; DNA) which causes milkmaid's blisters |
| What is the treatment for molluscum contagiousum (Poxvirus; DNA)? | Leave them alone! What did they ever do to you? |
| #1 cause of fatal diarrhea in children, especially in the winter months | Rotavirus (Reovirus; RNA) |
| PicoRNAviruses that cause meningitis and myocarditis | Echovirus and coxsackievirus |
| PicoRNAvirus that affects the motor neurons of anterior horn and causes paralysis | Poliovirus |
| PicoRNAvirus that causes acute viral hepatitis | HepA |
| Hepvirus (RNA) that causes a form of hepatitis that is enterically-transmitted and is associated with epidemics and a high mortality rate in pregnant women | HepE |
| What are the flaviruses (RNA)? | HCV, Yellow fever, Dengue, St Louis encephalitis, and West Nile virus (flavi means yellow, so think yellowing and jaundice) |
| What are the retroviruses (have reverse transcriptase to synthesize DNA from RNA)? | HIV-AIDS and HTLV (Human T-lymphotropic Virus)- T cell leukemia |
| German measles | Rubella (Togavirus; RNA) |
| Eastern and Western equine encephalitis | Togavirus (RNA) |
| Common cold | Coronavirus (RNA) and Rhinovirus (Picornavirus; RNA) |
| Colorado tick fever | Reovirus (RNA) |
| Aseptic meningitis in a kid from a swimming pool | Echovirus (picornavirus; RNA) |
| Aseptic meningitis, herpangina, febrile pharyngitis, hand, foot, and mouth disease, myocarditis | Coxcackievirus (picornavirus; RNA) |
| Viral gastroenteritis | Norwalk virus (calcivirus; RNA) |
| Why are patients susceptible to a secondary infection with strep pneumo, staph aureus, or H flu after infection with influenza? | B/c of virally induced damage to mucociliary clearance mechanisms in respiratory epithelium |
| What virus causes bronchiolitis in babies? What is the treatment of choice? | RSV (paramyxovirus; RNA). Tx is ribavirin |
| Rubeola | Measles (paramyxovirus; RNA) |
| Brassy, low-pitched cough with an infected larynx | Croup (PARAinfluenza; PARAmyxovirus; RNA); cough is also described as a barking seal cough |
| Virus that produces Ebola/Marburg hemorrhagic fever | Filovirus (RNA) |
| Virus assoc'd with animal urine; may cause hemorrhagic fever and penumonia | Hanta virus |
| Which liver tropic virus is a part of the deltavirus family? | HepD |
| How are all picornaviruses spread? What is the one exception? | All are enteroviruses, so they are spread via the fecal-oral route. Rhinovirus is the one exception. Picornaviruses include poliovirus, echovirus, rhinovirus, coxsackievirus, and HAV |
| Why is rhinovirus, unlike the other picornaviruses, unable to infect the GI tract? | It is acid lable, so it gets destroyed by stomach acid. |
| Transmitted by Aedes mosquitos; high fever, black vomitus, and jaundice | Yellow fever virus(Flavivirus; RNA) |
| High fever, jaundice, white coat on center of tongue with red at the tips and sides of the tongue | Yellow fever virus (Flavivirus; RNA) |
| Child with severe greenish diarrhea in the winter months | Rotavirus (Reovirus; RNA); very contagious! |
| How does rotavirus cause diarrhea? | VIllous destruction with atrophy leads to decreased absorption of Na and water |
| What influenza antigen is responsible for promoting viral entry? | HemaggLUTININ (LUTS INfluenza IN!) |
| What influenza antigen is responsible for promoting progeny virion release? | NEURaminadase (like a NEURsery/nursery letting the little progeny/kiddies out at the end of the day!) |
| What change in the influenza virus is responsible for the need to get a new flu shot each year? | Genetic drift (minor; epidemic; changes based on random mutation). Compare to genetic shift which is reassortment of viral genome, major, and pandemic. |
| Fever, postauricular tenderness, lymphadenopathy, fine truncal rash | German measles (caused by Rubella which is a togavirus) |
| Virus that causes mild infection in children, but has serious congenital sequelae like PDA and pulmonary stenosis in neonates | Rubella (a togavirus that causes German measles in children) |
| Which group of viruses contain a surface F (fusion) protein which causes respiratory epithelial cells to fuse and form multinucleated cells? | Paramyxoviruses (parainfluenza/croup, mumps, measles, RSV) |
| What drug is used in RSV to neutralize the surface F (fusion) protein? | Palivizumab |
| Koplik spots, cough, coryza, conjunctivitis | Rubeola (measles) virus (a paramyxovirus); also includes a head-to-toe rash which includes hands and feet |
| Parotitis, Orchitis, and aseptic meningitis; may lead to sterility in post-pubescent boys | Mumps virus (paramyxovirus; RNA) |
| Negri bodies in cytoplasmic inclusions in neurons (commonly in Purkinje cells of cerebellum) | Rabies virus (Rhabdovirus; RNA) |
| Bullet-shaped capsid | Rabies (think about Old Yeller getting a bullet b/c he had rabies) |
| Fever, malaise--> Agitation, photophobia, hydrophobia--> paralysis, coma--> death | Rabies virus (Rhabdovirus; RNA) |
| What should occur immediately upon exposure to a rabies vaccine, even though the incubation period of the virus lasts for weeks to months before symptom onset? | Prophylactic vaccination |
| What is the path of infection of the rabies virus? | Wound--> neuron axons--> salivary glands |
| How does the rabies virus travel to the CNS? | Travels to the CNS by migrating in a retrograde fashion up the n axons |
| A patient presents with restlessness, agitation, and dysphagia which progresses to a coma 30-50 days following an exposure to cave bats. | Rabies virus (Rhabdovirus; RNA) |
| Rash that starts at head and moves down to feet, disappearing in the same sequence as it developed | Measles (think of a can of red paint being poured over the patient's head; as it drips down the body to the feet, it comes off of the head, shoulders, etc.); Paramyxovirus: Rubeola |
| Fine truncal rash only lasting for 3 days | Rubella (Togavirus)= German (3 day) measles |
| Rash that develops only after a fever breaks | Roseola (HHV6) |
| Which virus can have a rare complication of sclerosing encephalitis years after apparent recovery from the initial infection? | Measles (paramyxovirus; RNA); oligoclonal bands of antibodies to the virus are found in the CNS while antibodies to the M component of the virus are not |
| Name that hepatitis!: short incubation, no carriers | HepA (picornavirus); fecal oral route of transmission |
| What type of food is the typical culprit of HAV infection? | Raw or steamed shellfish |
| Do children with HAV infection typically present with jaundice? | No; they are usually anicteric (no jaundice) |
| Name 5 ways that HAV can be inactivated. | 1. Water chlorination 2. Bleach 3. Formalin 4. UV irradiation 5. Boiling to 85C for 1min |
| Close contacts of an HAV infected person should be prophylaxed with _______. | Immunoglobulin |
| Name 3 histological findings seen in all cases of acute viral hepatitis. | 1. Diffuse ballooning degeneration (heaptocyte swelling) 2. Mononuclear cell infiltrates 3. Councilman bodies (eosinophilic apoptotic hepatocytes) |
| What is the MC cancer caused by HepB and HepC? What is the assoc'd tumor marker that should be regularly checked in infected patients? | Hepatocellular carcinoma; AFP |
| Name that hepatitis!: Primarily a sexual transmission | Hep B (You get it in Bed! Lucky you!) |
| Name that hepatitis!: Primarily transmitted in blood | Hep C (the Clean one) |
| Name that hepatitis!: The only one that is a DNA virus | Hep B |
| Name that hepatitis!: Virion enzyme is a DNA-dependent DNA polymerase | Hep B |
| What is the path of synthesis of progeny ds DNA in Hepatitis B virus? | ds DNA--> template + RNA--> progeny ds DNA |
| Name that hepatitis!: Common cause of hepatitis among IV drug users in US. | Hep C |
| Name that hepatitis!: Requires HBsAg as its envelope | Hep D |
| Name that hepatitis!: Enteric transmission, causes waterborne epidemics, high fatality rate in pregnant women | Hep E |
| Name that hepatitis!: Predispose patients to chornic active hepatitis, cirrhosis, and hepatocelluar carcinoma | Hep B and C |
| Why are hepatitis A and E able to infect via the fecal-oral route? | B/c naked viruses do not rely on an envelope, they are not destroyed in the gut. |
| Congenital cataracts (white pupils- bilateral unlike retinoblastoma), sensory neural deafness, and PDA | Congenital rubella (German measles), a togavirus (RNA) |
| How can congenital rubella be prevented? | Giving MMR (a live, attenuated vaccine) to women >4 mos b/f getting pregnant |
| Interpret that hepatitis serologic marker!: Anti-HAV Ab (IgM) | Active infection with HepA |
| Interpret that hepatitis serologic marker!: Anti-HAV Ab (IgG) | Prior HAV infection (IgG= Gone!) ; protected against future infection |
| Interpret that hepatitis serologic marker!: HBsAg | Infected with HepB |
| Interpret that hepatitis serologic marker!: anti-HBsAg | Immunity to HepB (either recovered from an infection or received passive immunization like a vaccine) |
| Interpret that hepatitis serologic marker!: anti-HBcAg IgM | acute or recent HepB infection |
| Interpret that hepatitis serologic marker!: anti-HBcAg IgG | chronic HepB |
| Interpret that hepatitis serologic marker!: HBeAg | Active HepB infection; making lots of viruses so you have high transmissibility |
| Interpret that hepatitis serologic marker!: anti-HBeAg | Low transmissibility |
| Which hepatitis serologic marker is positive during the window period? | Anti-HBcAg (IgM) |
| Which hepatitis serologic marker first apepars before the onset of symptoms, peaks when the patient is most ill, and then becomes undetectable in 3-6 mos? | HBsAg |
| What is the only hepatitis serologic marker that will be positive in patients who were only vaccinated against HepB? | Anti-HBsAb |
| Why don't neonates with HepB infection present with severe hepatic injury? | Their immune system is still too immature to mount a major response against the virus, so the damage is minimal (until they develop a stronger immune response). |
| Breakbone fever: musle/joint pain, headache, retro-orbital pain | Dengue fever |
| Tourniquet test (WHO field test for diagnosing hemorrhagic fever) can diagnose this illness | Dengue fever |
| Meningitis, encephalitis, m weakness, flaccid paralysis (via anterior horn involvement), alterations in consciousness, and possibly death; birds are the reservoir and mosquitoes are the vectors | West Nile virus; tx is supportive |
| URI, GI symtpoms (diarrhea), fever, pancytopenia, elevated aminotransferases (AST, ALT) | Avian influenza; H5N1 (spread from bird--> human) |
| What is the treatment for avian influenza/H5N1? | Oseltamavir |
| Typical flu symptoms with GI symptoms | H1N1 influenza/swine flu |
| What is the treatment for H1N1 influenza/swine flu | Oseltamivir or zanamivir to high risk or severely ill patients |
| What is the strain makeup of H1N1? | 2 swine flu strains, 1 human strain, and 1 avian strain. Yummy! |
| Steeple sign on x-ray | parainfluenza/croup (RNA virus) |
| Can ribavirin be used to treat RSV bronchiolitis? | Only in adults; in children ribavirin should NOT be given; give kids albuterol or racemic epinephrine and oxygen |
| Name that antiviral!: Blocks viral penetration/uncoating (M2 protein) | Amantadine (a man to dine takes off his coat) and rimantadine |
| WHy can amantadine be used to treat Parkinson's disease? | Because it causes the release of dopamine from intact nerve terminals |
| Why is amantadine rarely used to treat the flu? | 90& of all influenza A strands are resistant; may be given as a prophylaxis though |
| Name that antiviral!: Inhibits influenza neuraminidase (decreases release of progeny virus) | Zanamivir and oseltamivir |
| What are zanamivir and oseltamivir used to treat? | Influenza A and B |
| Name that antiviral!: Inhibits syntehsis of guanine nucleotides by compeitively inhibiting IMP dehydrogenase | Ribavirin |
| What is ribavirin used to treat? | RSV (in adults only), chronic Hep C |
| What are the side effects of ribavirin? | Hemolytic anemia and severe teratogen (unrelated, but think of how ribavirin can't be used in kids. ribavirin is rotten for kids and bad for babies) |
| What are the treatments used for Hep C (2)? | Ribavirin and IFN alpha |
| Name that antiviral!: Monophosphorylated by HSV/VZV thymidine kinase. Preferentially inhibits viral DNA polymerase by chain termination | Acyclovir |
| What are the clinical uses for acyclovir? | treat HSV1/2, VZV, and EBV |
| Why are higher doses of acyclovir required to treat EBV? | Because EBV produces a different thymidine kinase than HSV and VZV do whic prevents it from easily converting acyclovir into its active metabolites. |
| Which agent should be used to treat herpes zoster? | Famciclovir |
| What toxicity can result if acyclovir is given IV? | Nephrotoxicity; hydration can help prevent this |
| What is the mechanism of resistance to acyclovir? | Lack of viral thymidine kinase (can't activate acyclovir) |
| Name that antiviral!: 5'-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase; preferentially inhibits viral DNA polymerase | Ganciclovir |
| What is the clinical use for ganciclovir? | CMV, espeically in immunocompromised patients |
| What is the mechanism of resistance to ganciclovir? | Mutated CMV DNA polymerase or lack of viral kinase |
| Name that antiviral!: Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. | Foscarnet (pyroFOSphate analog) |
| What differentiates foscarnet from acyclovir and ganciclovir? | Foscarnet does NOT require activation by viral kinase |
| What is the clinical application for foscarnet? | CMV retinitis in immunocompromised patients when ganciclovir fails and acyclovir-resistant HSV |
| What toxicity is seen with foscarnet? | Nephrotoxicity |
| What is the mechanism of resistance to foscarnet? | Mutated DNA polymerase |
| Which antiviral has the following toxicities: leukopenia, neutropenia, thrombocytopenia, and renal toxicity | Ganciclovir (more toxic to host enzymes than acyclovir) |
| How do interferons work as anti-viral therapy? | They are glycoproteins synthesized by virus-infected cells that block replication of both RNA and DNA viruses |
| Which interferon is used to treat chronic HepB and C, and Kaposi's sarcoma | IFN-alpha |
| Which interferon is used to treat MS? | IFN-beta |
| Which interferon is used to treat NADPH oxidase deficiency? | IFN-gamma |
| HIV envelope protein that mediates attachment to the host T cell | gp120 (the grabber) |
| HIV envelope protein that mediates fusion and penetration/entry into the host T cell | gp41 |
| How does HIV reverse transcriptase work? | Synthesizes dsDNA from RNA (HIV is diploid and has 2 molecules of RNA inside) |
| What enzyme allows HIV-synthesized dsDNA to be incorporated into the host genome? | Integrase |
| Which structural gene encodes for HIV reverse transcriptase? | pol |
| Which structural gene encodes for HIV gp120 and gp41 envelope proteins? | env (for envelope) |
| Which structural gene encodes for HIV p24/capsid protein? | gag (you gag when you try to swallow a capsule/capsid) |
| X4 HIV virus only uses which T cell receptor? | CXCR4 |
| R5 HIV virus only uses which macrophage receptor? | CCR5 |
| How does a homozygous CCR5 mutation affect HIV infection? | Makes host immune to infection |
| How does a heterozygous CCR5 mutation affect HIV infection? | Causes a slower course of infection |
| How is an HIV diagnosis made (what tests are used)? | ELISA (high sensitivity, so rules OUT with a - result). If ELISA is +, confirm with a Western blot assay (high specificity, so rules in with a + result). |
| How are HIV PCR/viral load tests used clinically? | To monitor effect of drug therapy on viral load or to see if the baby of an HIV + mother is truly infected (baby will have anti-gp120 Ab b/c they cross the placenta, but doesn't necessarily mean that they have the virus) |
| When are false negative tests to HIV most common? | In first 2 months b/c there is not enough Ab for test to be + yet. |
| What "count" is used to make an AIDS diagnosis? | CD4 <200. Also, HIV+ with an AIDS indicator condition (e.g., PCP pneumonia), or CD4/CD8 ratio <1.5 |
| What prophylaxis can be given to HIV + pregnant women to reduce transmissiblity to the baby? | Zidovudine (nucleosie analog) which is a reverse transcriptase inhibitor |
| What are the opportunistic infections of the brain seen in AIDS? | Cryptococcal meningitis, toxoplasmosis, CMV encephalopathy, AIDS dementia, and PML (JC virus) |
| CMV causes what opportunistic GI infection in AIDS patients? | CMV colitis |
| Which genital cancer is considered an opportunistic infection in AIDS patients? | Cervical cancer (HPV) |
| When CD4 counts drop below 50, what prophylaxis should only be administered in the case of a past history of cryptococcal meningitis? | Fluconazole |
| HIV patient with dementia | HIV encephalitis |
| Infectious protein with beta pleated sheets that can result in spongiform encephalopathy (e.g., Creutzfeldt-Jakob disease) | Prions |
| What is the mechanism of action of the -navir drugs? | Protease inhibitors: prevent maturation of new viruses which is normally mediated by HIV-1 protease (pol gene) which cleaves the polypeptide products of HIV mRNA into their functional parts. NAVIR TEASE a proTEASE. |
| What is the mechanism of action of nucleoside reverse transcriptase inhibitors? | Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain. |
| What is required for activation of NRTIs? | Thymidine kinase phosphorylation |
| Which NRTI is used for prophylaxis during pregnancy? | Zidovudine |
| What are the NRTIs? | Zidovudine, Stavudine, Didanosine, Zalcitabine, and Abacavir (Have you dined (vudine) with my nuclear (nucleosides) family?) |
| Which NRTIs can cause pancreatitis and peripheral neuropathy? | Didanosine, Zalcitabine, and Stavudine |
| Which NRTI causes megaloblastic anemia and bone marrow suppression? How can the bone marrow suppression be reversed? | Zidovudine; treat bone marrow suppression with G-CSF and erythropoietin |
| Which HIV anti-viral class causes lactic acidosis? | NRTIs |
| Which HIV anti-viral class causes a rash? | NNRTIs |
| Which HIV anti-viral class causes hyperglycemia (due to increased insulin resistance; may cause diabetes), GI intolerance, and lipodystrophy? | Protease inhibitors (navirs) |
| Which protease inhibitor causes thrombocytopenia? | Idinavir |
| How are non-nucleoside reverse transcriptase inhibitors (NNRTIs) different from nucleoside reverse transcriptase inhibitors (NRTIs)? | NNRTIs bind to reverse transcriptase at a site different from NRTIs and do NOT require phosphorylation to be active or compete with nucleotides. NNRTI binding is non-competitive. |
| What are the NNRTI drugs? | Nevirapine, Efavirenz, and Declaviridine (NEVIR EFIR DELAVIR <never ever deliver> nucleosides; all have "vir" in the middle) |
| What is the mechanism of action of enfuvirtide? | Binds viral gp41 subunit to inhibit conformation change required for fusion with D4 cells, blocking entry and replication (enFUvirtide is a FUsion inhibitor) |
| Which HIV antiviral carries an increased risk of bacterial pneumonia? | Enfuvirtide (may also cause hypersensitivity reaction at site of subq injection) |
| Which anti-mycobacterial drug should never be used with protease inhibitors? What drug should be used instead? | Rifampin (revs up p450 so decreases serum levels of protease inhibitors); use rifabutin instead |
| What is the MC outcome of HepB infection in an adult? | Complete resolution (not progression to cirrhosis or cancer) |
| From which cells does Kaposi's sarcoma tumor arise? | Mesenchymal cells |
| What causes hepatocyte damage in HepB? | The presence of viral HBsAg and HBcAg on the cell surface stimulates the host's cytotoxic CD8+ T lymphocytes to destroy the infected hepatocytes. Remember that the HepB virus itself does not have a cytotoxic effect, and that the Ab are neutralizing. |
| Name 3 causes of esophagitis (dysphagia and/or odynophagia) in HIV. | 1. Candida albicans 2. HSV-1 3. CMV |
| Dysphagia and odynophagia in an HIV patient with yeast cells and pseudohyphae that invade mucosal cells on histologic exam. | Candida albicans--> esophagitis |
| Dysphagia and odynophagia in an HIV patient with punched out ulcers containing eosinophilic intranuclear inclusions in multinucleate squamous cells at the ulcer margins. | HSV-1--> esophagitis |
| Dysphagia and odynophagia in an HIV patient with linear ulceration and both intranuclear and cytoplasmic inclusions | CMV--> esophagitis |
Created by:
sarah3148
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