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CELL MICRO S1 > Viruses Blood and Insect borne > Flashcards

Viruses Blood and Insect borne Flashcards

1
Q

give some examples of physical barriers to infection

A
  • skin (physical barrier)
  • stomach pH
  • GI flora
  • mucous in lungs
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2
Q

how do blood and insect borne viruses infect?

A

they get past skin as a barrier

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3
Q

what are the 2 shared features of blood and insect borne viruses?

A

1) direct introduction to bloodstream

2) require high levels of viraemia (presence of blood in bs)

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4
Q

what are the 4 unique features of blood and insect borne viruses?

A

1) different entry into the bs (insect bite, skin damage, medical)
2) cell/tissue tropism may be different (blood cells/liver cells)
3) clinical symptoms may vary by virus
4) epidemiology (person to person vs intermediate host transmission)

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5
Q

what is a tropism?

A

cells/tissues of a host that support growth of a particular tissue

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6
Q

how much of blood is plasma? what does it do?

A
  • ~1/2 is plasma
  • mostly water, ions to maintain isotonic
  • proteins
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7
Q

what are the formed elements of blood?

A
  • mostly RBC
  • platelets
  • leukocytes
  • neutrophils etc
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8
Q

give 4 examples of blood borne viruses?

A

1) HIV
2) Hep B,C,D
3) HCMV (human cytomegalovirus)
4) HTLV1 (human T-cell lymphotropic virus)

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9
Q

what are the common ways of transmission for blood borne viruses?

A
  • unprotected sex
  • mother to baby
  • sharing injecting equipment
  • contaminated blood transfusions & organ transplants
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10
Q

where are viruses that cause blood borne disease found in the body?

A
  • blood
  • semen
  • vaginal secretions
  • other fluids that may contain blood (but aren’t supposed to) i.e urine, saliva
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11
Q

what is the family of HIV?

what is the genus?

A

Retroviridae

Lentivirus

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12
Q

what are 2 strains of HIV?

A

HIV-1 (global)

HIV-2 (West Africa)

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13
Q

how does HIV cause long term persistence?

A

integrates into the host genome

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14
Q

what is the tropism for HIV?

A

immune cells: CD4+ T cells, macrophages and dentritic cells

- infection results in DESTRUCTION OF CD4+ T cells

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15
Q

what does initial infection w/ HIV cause?

A

mild symptoms

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16
Q

what happens after long incubation periods in HIV?

A

causes AIDS (acquired immunodeficiency syndrome)

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17
Q

how do patients with AIDS die? how?

A

die from opportunistic infections
(HIV itself doesn’t kill)
- CD4+ T cells (normally 600 cells/mm3) are attacked but if AIDS, it drops below 200 cells/mm3

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18
Q

what can AIDS cause?

A
  • HIV related Encephalopathy
  • Cytomegalovirus Retinitis
  • Atypical Pneumonia
  • Chronic Intestinal Cryptosporidiosis
  • Invasive Cervical Cancer
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19
Q

describe the progression of HIV to AIDS

A 
week 0 (point of infection)
- replication of virus begins

week 6

  • peak in virus replication
  • ACUTE phase
  • seeding in all lymphoid organs
  • non specific symptoms
  • dip in CD4+Tcells

week 12

  • virus paritially controlled by immune syst
  • increase in CD4+ T cells
  • but virus NOT CLEARED
  • virus integrates into CD4+ T cell genome

week 12–> year 7

  • clinical latency
  • CD4+ T cellcount decreases
year 7 onwards
- CD4+ T cells reach below 200 cells/mm3
AIDS
-less able to fight infection
- immune system less able to control HIV O massive increase in HIV replication

DEATH (v late, 9/10 years)

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20
Q

are there vaccines for HIV?

A

no

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21
Q

what is the treatment for HIV?

does it cure?

A

highly active antiretroviral therapy (HAART)

  • combination drug therapy
  • prevents progression to AIDS
  • not curative
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22
Q

Hep B, C and D are all what?

A

chronic, without integration into the host genome

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23
Q

what is the family and genus of Hep C?

A

Flaviridae

Hepacivirus

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24
Q

what is the family and genus of Hep B?

A

Hepadnaviridae

Orthohepadnavirus

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25
Q

Hep D is what?

A

a VIROID (subviral satellite)

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26
Q

describe Hep D

A
  • can only replicate in the presence of HBV
  • transmitted with HBV, or to a chronic HBV patient
  • inc SEVERITY of HBV disease
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27
Q

what is the tropism of Hepatitis blood borne?

A
  • liver cells (hepatocytes)

- infection causes chronic liver inflammation

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28
Q

what are the symptoms of intial infection with Hep?

A

mild symptoms

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29
Q

what does a long incubation period cause in Hep?

A

liver failure and cancer

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30
Q

how does Hep progress?

A
  • initial inf
  • replication in liver
    75-85% get chronic Hep: inflammation of liver causes FIBROSIS
  • 20-25 years later
    CIRRHOSIS (extensive scarring, loss of blood flow, reduced liver function
  • 25-30 years later
    HCC (hepatocellular carcinoma)
    ESLD (end stage liver disease)
    Death
    Hepatocellular carcinoma
    end stage liver disease
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31
Q

is there a vaccine for Hep C?

A

no

32
Q

what is the treatment for Hep C? how long for?

does it cure?

A
  • direct antiviral drugs
  • 12 week treatment
  • curative
  • expensive
33
Q

how is Hep C prevented?

A

good medical practice (screening of blood supply, no reuse of needles)

34
Q

is there a vaccine for Hep B?

A

yes, also protects against HDV

35
Q

what is the progression of HCV?

A
  • initial inf
  • 1-3 weeks viral particles in bs due to replication
  • jaundice/flu like

MAY RECOVER FROM THIS if antibodies formed

IF NOT
continuous replication
20-30 years later, liver damage causes death

36
Q

what can transmit arthropod borne viruses?

A

1) insects
- mosquitos
- sandflies
- midges
2) ticks

37
Q

what are the major insect borne viruses that affect humans?

A
  • Flaviviruses genus Flavivirus
  • Alphavirus
  • Bunyavirus
  • Rhabdovirus
38
Q

why are arboviruses limited to certain regions?

A

they are limited to the area in which the vector is found

39
Q

what is the name of the human-vector-human cycle of mosquito virus transmission?

A

urban epidemic cycle

40
Q

what is the enzootic cycle in mosquito borne transmission?

A

transmission in the wild, mosquitos—> non-human animals

this can spill over to humans (DEAD END HOST)

41
Q

what is the epizootic cycle in mosquito borne transmission?

A

spillover of the enzootic cycle into domesticated animals, then possibly spill over to humans (DEAD END HOST)

42
Q

what is a dead end host?

A

one that won’t transmit the disease on further

43
Q

what is the species of mosquito that causes yellow fever?

A

Aedes aegypyti

44
Q

Aedes albopictus is called what? what is it more tolerant to?

A

Asian tiger mosquito

more tolerant to cold

45
Q

where are New World Alphaviruses found? give an example of one

A

Americas

Venezuelan Equine Ecephalitis

46
Q

what do New World Alphaviruses cause generally?

A

encephalitis

47
Q

where are Old World Alphaviruses found? give an example of one

A

Africa, Asia

Chikungunya

48
Q

what do Old World Alphaviruses cause generally?

A

Arthiritis

49
Q

what is the family of Chikungunya virus?

A

Togaviridae

50
Q

what is the genus of Chikungunya virus?

A

Alphavirus

51
Q

what is the tropism for Chikungunya virus?

A

broad

  • immune cells (macrophages & dendritic cells)
  • fibroblasts (connective tissue)
  • endothelial (lining of blood vessels)
  • myocytes
52
Q

what are the symptoms of inital Chikungunya virus?

A

acute inital

some develop CHRONIC ARTHIRITIS (lasts ~2 years)

53
Q

what transmits Chikungunya virus?

A

Ae. aegypti, Ae. albopictus

via urban transmission

54
Q

where is Chikungunya found?

A

worldwide

55
Q

is there vaccine/treatment for Chikungunya virus?

A

no, only prevention via mosquito control

56
Q

what are the symptoms of Chikungunya?

A
  • fever
  • headache
  • rash
  • myalgia
  • ARTHIRITIS
57
Q

describe the infection life cycle of Chikungunya?

A
  • infected mosquito bites human, virus introduced into skin and bloodstream
  • virus replicates in fibroblasts of dermis and disseminates through bs to tissues
  • viral REPLICATION in target tissues (muscle, liver, joints, spleen, meninges in neonates & immunocompromised)
  • inflammation of joints
58
Q

what family and genus is Venezuelan equine encephalitis (VEE)?

A

Togaviridae Alphavirus

59
Q

what is the tropism of VEE?

A
  • immune cells and CNS
  • initial replication in DENDRITIC cells in blood
  • inf of PNS (nose, mouth)
  • spread along nerves to CNS
60
Q

is there persistence of VEE?

A

no, acute inf only

61
Q

what is the major symptom of VEE? what are other symptoms?

A

ENCEPHALITIS

  • severe headache
  • photophobia
  • chills
  • malaise
  • fever etc
62
Q

how did VEE emerge into humans?

A

the virus can infect multiple mosquito species (Culex)

63
Q

what is the enzootic cycle of VEE?

what changes when there is an outbreak of VEE?

A

Culex breeds in permanent water sources

- flooding attracts new types of mosquitos that can transmit the virus to human (inc in population)

64
Q

in VEE outbreaks tend to occur in what animal before humans?

A

horses (hence name V EQUINE E)

65
Q

in VEE humans are wjat kind of host?

A

dead end host

  • VIRAEMIA IS HIGH
  • mosquitos involved in transmission do NOT bite humans often enough to sustain urban human transmission cycles
66
Q

are there vaccines for VEE?

how else can VEE be prevented?

A

veterinary vaccine for horses

prevented by mosquito control

67
Q

what is the family and genus of the virus that causes West Nile virus?

A

Flaviviridae Flavivrus

68
Q

what is the tropism of West Nile virus?

A

immune cells, endothelial cells, and CNS

69
Q

where is initial replication of West Nile virus?

where does it spread to?

A

endothelial cells, monocytes, macrophages and dendritic cells
spread to neurones

70
Q

is West Nile virus persistent?

A

no

71
Q

what isWest Nile virus transmitted by?

A

Culex spp mosquitos

72
Q

where is West Nile virus found?

A

worldwide

73
Q

what are the natural vertebrate hosts for West Nile virus? how does it infect humans?

A

birds (epizootic)

sporadic spillover to humans/horses (dead end hosts as VIRAEMIA IS NOT HIGH ENOUGH FOR TRANSMISSION BACK TO HOST).

74
Q

what are the symptoms of West Nile virus?

A 
in 20-30% 
- fever
- headache
- EYE PAIN 
- MACULOPAPULAR RASH 
(self lim)
NEUROINVASIVE (1/150 cases)
- encephalitis 
- meningitis
- movement disorders
- long term cognitive and neurological impairment 
- 10% mortality (high in older people)
75
Q

how is West Nile virus treated?

A

no specific antiviral or vaccine

can be prevented by mosquito control

CELL MICRO S1 (16 decks)

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