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Pharm Y2S1 > Viral Infections > Flashcards

Viral Infections Flashcards

1
Q

What causes rabies?

A

Lyssavirus transmitted via bites from infected animals

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2
Q

What causes yellow fever?

A

Transmittion of arbovirus via mosquito vectors

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3
Q

What is the first stage of yellow fever?

A

Lasting up to 6 days- fever, muscle pain, headaches

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4
Q

What is the second stage of yellow fever?

A

50% survival- jaundice, abdominal pain, haemorrhage

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5
Q

What are the two malaria species that pose the greatest threat?

A

P. falciparum and P vivax

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6
Q

How is malaria transmitted?

A

The female anopheles mosquito acts as a vector- 30 of 400 species take on this role.

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7
Q

What is the first stage of malarial febrile paroxysms?

A

Vasoconstriction
Shivering
Rapid increase in temperature to 41 degrees

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8
Q

What is the second stage of malarial febrile paroxysms?

A

Delirium lasting 2-6 hours

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9
Q

What is the third stage of malarial febrile paroxysms?

A

Sweating

Fatigue

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10
Q

What complications may occur if over 2% of red blood cells become infected with malaria?

A

Cerebral malaria

Black water fever, leading to renal failure

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11
Q

What is the treatment for malaria?

A

Quinine, malarone or raimet

Artemensin combined with one of the above minimises resistance.

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12
Q

What is used to treat resistant malaria?

A

Chloroquine

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13
Q

What is the disadvantage of quinine?

A

Very toxic in overdose

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14
Q

What is the disadvantage of raimet?

A

Prolongs QT interval

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15
Q

What are the effects of tick borne encephalitis?

A

Influenza like symptoms

Inflammation of the brain and spinal cord

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16
Q

What is the most common cause of gastroenteritis in the UK?

A

Norovirus

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17
Q

Describe the structure of norovirus.

A

27nm in size with icosahedral nucleocapsid. Small non-enveloped virions. Part of the Caliciviridae family

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18
Q

Why is norovirus so infectious?

A

It has an extremely low infectious dose

<10 virions to infected 50% of individuals

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19
Q

What are the symptoms of norovirus?

A 
Sudden onset nausea
Projectile vomiting
Diarrhoea
Abdominal pain
Headache
Myalgias
Malaise
Lasting 24-72 hours
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20
Q

What causes diarrhoea in norovirus?

A

Nutrient malabsorption with enzymatic dysfunction ate the brush border.

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21
Q

What causes vomiting in norovirus?

A

Virus mediated changes in gastric motility and emptying.

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22
Q

What is the general life cycle of a virus?

A

Virion absorbed into host cell
Virus penetrates cell and uncoats
Viruses replicate certain components to assemble in host cell
Components released by budding
Spread via cell-cell contact
Both abortive and productive infections can lead to cell death

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23
Q

Describe the structure of influenza viruses.

A

Have single stranded RNA, three subtypes are infectious to humans. Antigenic surface proteins include neuraminidase and haemagglutinin.

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24
Q

What is the role of haemagglutunin in influenza?

A

Receptor binding site that attaches to sialic acid containing receptors on host cells. Influenza visions can then be internalised by endocytosis.

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25
Q

What is the role of neuraminidase in influenza?

A

Cleaves sialic acid so newly formed virions are able to spread to other cells.

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26
Q

What are the roles of M proteins in influenza?

A

M1 is significant in viral assembly
M2 channels transport protons to control pH, low pH triggers the fusion of viral and end-somali membranes allowing RNA to be transported to the nucleus of the host cell.

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27
Q

What is antigenic drift?

A

Slight modification of a virus to evade the immune system.

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28
Q

What is antigenic shift?

A

Radical modification of a virus to evade the immune system.

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29
Q

What is amantadine?

A

A synthetic tricyclic amine that at high concentrations inhibits the uncoating of influenza virus within fusion vacuoles and at low concentrations inhibits cell penetration. Used to help ease symptoms of influenza.

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30
Q

What is oseltamivir? How does it work?

A

Transition state inhibitor used as a sialic acid analogue to inhibit neuraminidase on the influenza virus. It is an ester prodrug taken orally.

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31
Q

How do primary Herpes simplex infections occur?

A

Entry via a break in the mucus membrane/skin

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32
Q

How does the Herpes virus evade host immune system?

A

Enters via peripheral sensory nerves and migrates along axons to the CNS. Virus then becomes latent and reactivation leads to recurrent disease as it travels back to the surface of the body to replicate, causing tissue damage.

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33
Q

What is varicella zoster?

A

Chicken pox, infection occurs via respiratory tract or conjuctiva eventually spreading to the blood stream.

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34
Q

What occurs after primary infection with varicella zoster?

A

The virus persists in the sensory ganglia of the CNS.

35
Q

What is zoster virus?

A

Shingles, reactivation of varicella zoster virus after many years leading to infection and tissue damages. More serious when involving optic or cranial nerves.

36
Q

What is zoster virus treated with?

A

Aciclovir

37
Q

What is Epstein-Barr?

A

A virus shed in saliva which can exist asymptomatically with T cell control or become acute mononucleosis (glandular fever).

38
Q

What is mononucleosis?

A

Glandular fever. Presents with fever, sore throat, fatigue, resolves itself within 2-6 weeks.

39
Q

What is idoxuridine?

A

First effective antiviral developed in 1962, monophosphate active form produced within the cell. Used topically due to toxicity.

40
Q

What is acyclovir? How does it work?

A

A purine analogue, triphosphate form is a selective viral DNA polymerase inhibitor that incorporates into the growing DNA strand causing early termination. Cellular thymidine kinases have lower affinity than viral counterparts.

41
Q

What is ganciclovir?

A

Active against cytomegalovirus, same action as acyclovir.

42
Q

What is penciclovir?

A

A bioisostere of ganciclovir.

43
Q

What is valaciclovir?

A

A valine ester prodrug of aciclovir used for skin/mucus membrane infections.

44
Q

What causes resistance to acyclovir?

A

Some viruses lack thymidine kinases.

45
Q

What is cidofovir?

A

Monophosphate bioisostere phosphonomethylene, mainly used in cytomegalovirus retinitis.

46
Q

Describe the structure of mature HIV.

A

Bar shaped electron dense core counting the viral genome- two short RNA strands, reverse transcriptase, proteases, ribonuclease and integrase. Encased in an outer lipid layer of GPs 120 and 41.

47
Q

What are the primary cell targets of HIV?

A 
Blood monocytes
Tissue macrophages
NK cells
Lymphocytes
Dendritic cells
Haematopoietic stem cells
Epithelial (GI)
Endothelial
48
Q

Describe the mechanism of HIV infection.

A

Binding of CD4 and gp120 to release gp41 which facilitates the fusion of the viral envelope to the cell membrane. The provirus is then replicated by the host to release new virions. Replication site often shifts from inflammatory/peripheral mononuclear cells to lymphoid tissues. RNA genome is reverse transcribed into cDNA and integrated into the host cell genome.

49
Q

Why is vaccination of HIV difficult?

A

Mutation of HIV-1 occurs rapidly

Cells do not retain their antigenicity when killed.

50
Q

Describe the structure of hepatitis B virus.

A

Circular DNA with a longer negative strand. 42-47nm virions, blood also contains 20nm spheres with HBV surface antigens.

51
Q

How does the hepatitis B virus replicate within the host?

A

The virus multiples via RNA made by a host enzyme, DNA is transferred to the nucleus by chaperone proteins. Viral DNA is transformed to cccDNA to serve as a template. The mRNA is then synthesised back to DNA using the vision P protein.

52
Q

What are the symptoms of hepatitis B?

A 
May not occur until up to 30 years post infection
Jaundice
Fatigue
GI symptoms
Abdominal pain
53
Q

What is hepatitis B?

A

Viral infection that causes scarring of the liver and liver failure.

54
Q

What immune response affects hepatitis B?

A

Immune response during infection causes hepatocellular damage and viral clearance. Cytotoxic T cells are particularly associated with liver injury

55
Q

What is likely to occur in the case of an HIV infected pregnant mother without intervention?

A

20% risk of passing on the infection during childbirth in sAg positive.
Increases to 90% if also eAg positive.

56
Q

What drugs can be used to reduce replication of hepatitis B?

A 
Lamivudine
Adefovir
Tenofovir
Telbivudine
Entecavir
57
Q

Give examples of HIV transmission.

A

Sexual contact
Mother to child
Contaminated blood/needles
Occupational exposure

58
Q

What classifies AIDS?

A

CD4 cell count of <200/mm3 with one or more specific conditions classed as AIDs defining illnesses- PCP, TB, Kaposi’s sarcoma, CMV

59
Q

What is the treatment threshold for CD4 count in HIV?

A

< 350/mm3

60
Q

What are the likely signs in HIV when CD4 count is <50/mm3?

A 
MAI
Cryptococcal
CMV
Aspergillosis
Wasting
61
Q

What are the aims of antiretroviral therapy for HIV treatment?

A

Combination of at least three drugs to increase efficacy and reduce resistance. To be started after diagnosis regardless of CD4 count. Aim for viral load of <50 copies/mL.

62
Q

What are nucleoside analogue reverse transcriptase inhibitors?

A

HIV drugs that are phosphorylated intracellularly and halt DNA synthesis.

63
Q

What are the side effects of NARTi?

A

Lactic acidosis

Hepatic steatosis

64
Q

What are non-nucleoside analogue reverse transcriptase inhibitors?

A

HIV treatment that does not require phosphorylation before binding to reverse transcriptase to prevent DNA synthesis.

65
Q

What are the side effects of NNARTi?

A

CNS disturbance
Psychiatric disorders
Hepatitis
Rash

66
Q

What are protease inhibitors?

A

HIV treatment that binds to the active site of HIV protease preventing maturation of virions so they remain non-infectious.

67
Q

What are the side effects of protease inhibitors?

A

Hyperglycaemia
Hyperlipidaemia
Lypodystrophy- fat redistribution

68
Q

What are entry inhibitors?

A

HIV treatment that inhibits fusion, binding and entry in resistant HIV.

69
Q

What are integrase inhibitors?

A

HIV treatment that blocks incorporation of viral DNA into the host genome.

70
Q

What are the side effects of integrase inhibitors?

A

Muscle weakness.

71
Q

Give examples of NARTi

A

Zidovudine, abacavir, lamivudine

72
Q

Give examples of NNARTi.

A

Efavirenz, nevirapine, rilpivirine

73
Q

Give examples of protease inhibitors.

A

Atazanivir, darunavir, lopinavir, tipranavir

74
Q

Give examples of entry inhibitors.

A

Enfuvurtide, maraviroc

75
Q

Give examples of integrase inhibitors.

A

Raltegravir, elvitegravir

76
Q

What is HAART?

A

First line HIV therapy with two NARTi and one of NNRTI, boosted PI (with ritonavir) and II.

77
Q

What is HIV PEP?

A

Pre/post exposure prophylaxis recommended dependent on sexual/occupational risk.

78
Q

What is AZT?

A

Zidovudine, NARTi for HIV treatment, active IV or orally against HIV-1 and HIV-2.

79
Q

How does zidovudine work?

A

Deoxythymidine analogue that enters host cell via diffusion. N3 chain terminating group prevents further DNA extension during reverse transcription.

80
Q

When is efavirenz used in HIV treatment?

A

Active against HIV-1 and used with nevirapine to avoid resistance.

81
Q

What is saquanavir?

A

1st developed HIV protease inhibitor.

82
Q

What are the recommended 1st line drugs for HIV therapy?

A

NRTs- lamivudine and tenefovir.

Efavirenz

83
Q

What is enfuviritide?

A

HIV therapy that displaces components of the HIV fusion machinery.

Pharm Y2S1 (8 decks)

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