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Human Diseases > W4 16 viral infections: an overview > Flashcards

W4 16 viral infections: an overview Flashcards

1
Q

What are some important viruses to know?

A

Herpes simplex virus 1 and 2 - HSV-1 HSV-2
Hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Human immunodeficiency virus (HIV)
Also be aware of: human papilloma virus (HPV) and varicella zoster virus (VZV)

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2
Q

Characteristics of herpesviruses

A

Big viruses
Enveloped - by plasma membrane when virus buds out of affected cell
Double stranded DNA viruses - less accumulation of mutations (they have proofing)

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3
Q

How are herpes simplex virus 1 and 2 transmitted?

A

Oral to oral contact; HSV-1 in the sores, saliva, surfaces in or around the mouth

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4
Q

Are herpes simplex viruses 1 and 2 symptomatic or asymptomatic

A

Most oral and genital herpes infections are asymptomatic
Herpes infections are most contagious when symptoms are present
Transmission during asymptomatic outbreaks possible
Frequency of recurrence varies from person to person

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5
Q

What are some clinical manifestations of HSV-1

A

Encephalitis
Conjunctivitis
Oropharyngeal Herpes
Mucocutaneous disease (immunocompromised)
Primary genital herpes/recurrent herpes genetalis
Herpes whitlow

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6
Q

What are some clinical manifestations of HSV-2?

A

Mengingitis
Oropharyngeal Herpes
Perianal Herpes
Primary genital herpes/recurrent herpes genetalis
Herpes whitlow

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7
Q

HSV-1,2 and VZV are part of the alpha subfamily of herpes viruses. What is their target cell?

A

HSV1,2 mucoepithelial cells (eg lips where they are moist)
VSV epithelial cells

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8
Q

What are the 2 parts to a HSV1 life cycle?

A

Lytic cycle
Latency

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9
Q

What happens in the primary infection of HSV1?

A

Lytic cycle: Infection of mucoepithelial cells, then replication in cells. Infectious virus is released. Virus replication destroys the cells, as well as immune system destroying these cells.
Infected for life.

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10
Q

What happens in reactivation of HSV1?

A

Latency: immunological silent infection. Reactivated eg by UV light, weakened immune system. Replication in mucoepithelial cells and infectious virus released.

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11
Q

Where does HSV1 establish latency?

A

It invades sensory nerve endings, establishing latency in the trigeminal ganglion, so is silent here. Upon reactivation it travels back down the nerve to sensory nerve endings to replicate.

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12
Q

Where does HSV have latency?

A

Sacral ganglia

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13
Q

Latency is a unique property of HSV. What is the other?

A

Neurovirulence - invades and replicates in the CNS. Profound disease - rare but can happen causing severe neurological devastation, eg encephalitis.

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14
Q

Describe the whole process of HSV transmission/life cycle

A

Enters mucoepithelial cells through mucosal surface and replicates here
Virus is either released back into mucosal surface and transmitted in saliva, or will be released on the opposite side of the cell and enter the sensory nerve, entering up the ganglia where it will switch off all its virus expression to become antigenically invisible
Virus will stay there before it receives a signal that it can reactivate, moving back down the nerve, re-entering epithelial cells again and undergoing lyric replication, to be released into saliva and spread

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15
Q

What happens on a more sub cellular level in the lytic cycle of HSV?

A

Virus DNA replication
New progeny viruses made
Full range of virus proteins expressed
Cells become highly immunogenic

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16
Q

What happens on a more sub cellular level in the latency period of HSV?

A

No virus protein expression
Episomal DNA replicated with host cell DNA
Immunologically silent

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17
Q

What happens with HSV and immunocompromised patients?

A

They can’t control the virus as well
Eg transplant patients - severity related to type of immunosuppressive therapy, can lead to pneumonitis, esophagitis, gastritis
Eg HIV/AIDS patients - more exaggerated, more frequent, more resistant to antivirals

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18
Q

Characteristics of hep B virus

A

Enveloped
Very small virus
Double stranded DNA
Proteins allowing it to get into target cell. E antigen when virus actively replicating.

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19
Q

How can hep B be transmitted?

A

(Very infectious)
Perinatal transmission (mother to child at birth)
Parenteral transmission (blood)
Needle stick injury
Sexual
Infected body fluids (saliva, menstrual, vaginal, seminal fluids)
Medicinal/surgical/dental instruments

20
Q

High risk groups of getting hep B

A

Health care workers
Men who have sex with men
Blood tranfusion recipients
IV drug users
Infants of HBV carrier mothers
Recipients of solid organ transplants

21
Q

What is the antigen response in hep B virus?

A

When the virus is actively replicating, there is a spike in hepatitis B E antigen. Then will see antibodies develop to this antigen, and levels of the E antigen decline. IgM levels go up. After a while you see the development of antibodies to hepatitis B surface antigen.

22
Q

What are early markers of active HBV infection?

A

HBV DNA and HBeAg

23
Q

What will be seen in an effective host response against hep B?

A

Loss of HBeAg
Appearance of HBe antibodies
Clearance of HBV DNA and HBsAg

24
Q

What serological patterns are there for hepatitis B immunity - in natural exposure, vaccination, and acute infection?

A

Natural exposure - no surface antigens present, but antibodies to the core and surface antigens
Vaccination - no antibodies to core antigen and no surface antigens detectable, but antibodies to the surface antigen positive since the vaccine is made against this antigen.
Acute infection - antibodies to the core antigen (IgM), no surface antibodies (since this develops later), should have E antigens present, should have surface antigen positive, DNA positive.

25
Q

What happens in chronic HBV infection?

A

Surface antigen stays high since replication of the virus stays on
E antigen stays on for years (activating replicating)
Antibodies seen to core antigen
IgM comes up and goes down as expected
(Continued viral replication occurs)

26
Q

Serological pattern for chronic infection of HBV

A

IgG to core antigens. No antibodies for the surface antigen.

27
Q

Characteristics of the hep C virus

A

RNA virus
Often embedded and stuck to lipids

28
Q

Is there a vaccine to hep C?

A

No vaccine and highly prevalent

29
Q

How is hep C transmitted?

A

Blood borne virus
Injecting drug use/sharing injection equipment
Reuse or inadequate sterilisation of medical/surgical/dental equipment
Transfusion of unscreen blood and blood products
Sexual practices that lead to exposure to blood
Perinatal transmission (less common)

30
Q

Is hep C symptomatic or asymptomatic?

A

Acute infection - 80% are asymptomatic

31
Q

What are the symptoms of those with hepatitis C symptoms from acute infection?

A

20% of people experience fever, fatigue, decreased appetite, nausea, vomiting, abdominal pain, dark urine, joint pain, jaundice

32
Q

What are the symptoms from acute and chronic infection of hepatitis B?

A

Acute - jaundice and hepatitis
Chronic - cirrhosis and/or liver cancer

33
Q

What will 20% of those infected with hep C virus develop?

A

Cirrhosis and or liver cancer

34
Q

How is hep C diagnosed?

A

Most people don’t realise they’ve been infected, so antibody testing first
Positive result to this means a viral nucleic acid test will be needed to confirm current infection
If positive, check for cirrhosis

35
Q

What is the timeline for virus replication?

A

At the beginning, replication of virus, so can detect viral RNA, peaking and troughing over Yeats until eventual liver disease
Lagging behind this is antibodies to hepatitis C
In start period with new active replication, that you may or likely not see symptoms
When RNA goes above a certain threshold, you might see symptoms

36
Q

How many genotypes does HBC have?

A

Multiple genotypes because RNA viruses do not have proofreading capability when their viral nucleic acids are replicating, so can develop mutations and form new genotypes.

37
Q

What are the characteristics of HIV?

A

Enveloped, large virus
Glycoproteins embedded in membrane allowing it to enter target cell
Uses CD4 as main receptors

38
Q

Who is at risk of HIV?

A

Men who have sex with men
IV drug users
Sex workers and their clients

39
Q

Acute HIV infection symptoms

A

Most people unaware they have been infected fever, headache, rash, sore throat

40
Q

Factors of chronic infection

A

Asymptomatic/latent. HIV replicating at low levels. Can last for a decade or longer (some progress faster). Transmission. Eventually virus load greatly increases and CD4 T cell count drops.

41
Q

What is the T cell count in AIDS?

A

CD4 T cell count drops below 200cells/mm
Increased susceptibility to opportunistic - infections maximum survival approx. 3 years

42
Q

What are some AIDS-defining opportunistic infection?

A

Cryptococcal meningitis, pneumocystitis pneumonia, oesophageal candidiasis, Kaposi’s sarcoma

43
Q

How is HIV transmitted?

A

Bodily fluids: blood, breast milk, semen, vaginal secretions
Mother to child DURING pregnancy and delivery

44
Q

What are risk factors for HIV?

A

Unprotected anal or vaginal sex
Other STIs
Sharing contaminated needles, syringes etc
Receiving unsafe injections, blood transfusions, tissue transplantation etc
Accidental needle stick injuries

45
Q

What is viremia?

A

Virus starts to replicate itself. Can her a nucleic acid test positive here.

46
Q

What is the antigen production cycle for HIV?

A

Virus starts to replicate itself, at the same time p24 is produced.
After a lag phase is production of antibodies to the envelope
Then production of antibodies to the core proteins
Antibodies to the envelope will persist because the virus is always there
Antibodies to the core won’t persist because over time you reduce the amount of virus replication you are getting
Symptom-free period (chronic)
Just before the AIDs period is a lot of virus replication, so you see a lot of p24 antigen and viral RNA

47
Q

What is the treatment for HIV?

A

ART drugs - first line treatment
When resistant to drugs, second line treatment (doesn’t really go through in lec)

Human Diseases (75 decks)

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