Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > dsDNA Virus - Herpesviridae > Flashcards

dsDNA Virus - Herpesviridae Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Talk about Herpesviridae

A

1) Characteristics
1- Large group of linear dsDNA viruses
2- Have ENVELOPED POLYHEDRAL CAPSIDS
+ viral envelop interacts and fuses with the cell membrane to facilitate entry into cell
+ viral envelope acquired from the host cell’s membrane
+ Virus exits the cell via exocytosis or cell lysis
2) Most Prevalent DNA viruses:
-infection rates in the population : 50-90%
3) Often latent
- remain inactive inside infected cells for years
+ reactivation causes recurrence of the disease manifestations
+ Some insert in the host genome and potentially induce cancer.

2) Nomenclature of Herpesvirus

HHV- a number indicatinf the order of discovery

3) Infections of Human Herpesvirus 1 and 2
+ Often result in slow spreading skin lesions
+ Formerly known as Herpes simplex virus or HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Characteristics of HHV1 and 2

A

1) Often result in SLOW-SPREADING SKIN LESIONS
2) Formerly known as HERPES SIMPLEX VIRUS
or HSV
3) 2 species, genus Simplexvirus
+ Human Herpesvirus 1 (HHV-1)
+Human Herpesvirus 2 (HHV-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Sites of Herpesvirus Infections

A

1) Fever Blisters of Oral Herpes
- Viruses invades the mucous membrane of the lips
2) Genital Herpes
- Genitalia
3) WHitlow
- Broken skin of the finger
4) Trigeminal, Sacral or brachial Ganglia
- where they reamin latent
- via sensory nerve cells
- recurrent symptoms reactivates as a result of immunosuppression and travels down nerve cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Types of HHV-1 and HHV-2 infections

A

1) Oral Herpes:
-HHV-1
Fever blister or cold sores, and also herpetic gengivostomatitis or pharingitis: HHV-1 and HHV-2
- Flu like symptoms

2) Genital Herpes:
- HHV-2 (most) and HHV-1
- Painful lesions
- Transmitted sexually

3) Ocular Herpes:
- HHV-1
- Opthalmic branch of trigeminal nerve
- Conjunctivitis, pain, sensitivity to light

4) Whitlow
- HHV-1, HHV-2
- Children, health care workers

5) Neonatal Herpes
-HHV-2, life-threatening infection.
Mortality rate:
30% (oral or cutaneous)
80% (CNS)
- in utero or during birth
Prevention: Cesarean section

6) Others
- Herpes Gladiatorum in athleres (HHV-1)
- HHV1 and HHV-2 may also cause encephalitis, meningitis and pneumonia in immunosuppressed individuals (AIDs patients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Comparative Epidemiology and Pathology of HHV1 and HHV2

A

Usual diseases
HHV1- 90% of cold sores/ fever blisters, whitlow
HHV2 - 85% genital herpes cases

Mode of transmission
HHV-1 Close contact
HHV2- Sexual intercourse

Site of latency
HHV-1 Trigeminal and brachial ganglia
HHV-2 Sacral ganglia

Location of lesions
HHV-1 Face, mouth and rarely trunk
HHV-2 External ganglia and less commonly thighs, buttocks and anus

Other complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Epidemiology and Pathogenesis of HHV1 and HHV2

A

1) Worldwide
2) Active lesions are the usual sourcce of infections
3) Asymptomaitc carriers shed HHV-2 genitally
4) Transmission occurs through cracks or cuts in mucous membranes
5) Viral replication in peithelial cells leads to lesion formation
6) Virus spreads from cell to cell through synctia fromation: escape antibodies
7) HHV-1 infections typically occur via casual contact in children (80% by age 2 have been asymptomatically infected)
8) HHV-2 infections occur between ages 15 and 29 from sexual activity: common sexually transmitted disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Diagnosis of HHV1 and 2

A

1) Characteristic lesions are often diagnostic. Histology: Synctia. Serological testing: viral antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment of HHV1 and 2

A

1) Infections can be controlled with chemotherapeutic agents (nucleoside anaglogues: valaciclovir)
- limit duration of the lesions and reduce viral shedding
- do not cure the disease or elimionate latent virus`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Prevention of HHV1 and 2

A

1) Use of gloves can reduce exposure in health care workers

2) Sexual abstinence and sex between uninfected partners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Talk about HHV3

A

hkhkhkh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Characteristic of HHV3

A

Genus Varicellovirus (VZV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Infectiosn of HHV3

A 
1) Causes 2 diseases
1- Varicella 
\+ Called chicken pox
\+ Typically occurs in children
2- Herpes Zoster
\+ Called shingles
\+ Usually occurs in adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Epidemiology and Pathogenesis of HHV

A

1- Chickenpox is a highly infectious disease, virus shed before and during symptoms (respiratory droplets and fluid of lesions)
2- Virus enters the body through the respiratory tract or eyes
3- Virus travels via the blood from infection site throughout the body
4- Characteristics skin lesions appear 2-3 week safter infection: back, trunk - face, neck, limbs ( mouth, pharynx, vagina)
5- The disease is usually mild in children
6- Chicken pos in adults is typically more severe (stronger immune response)
7- Latent virus can reactivate, producing a rash know as shingles
+ Lesions occur along a band of skin called dermatome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Characteristics of Varicella/Chickenpox Lesions

A

1- Macules
2- Papules
3- Thin Walled Vescicles
4- Crusts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Latency and reactivation of Varicella-zoster virus

A

1- Initial infection:
- Viruses move up spinal chord
2-Latency
- in nerve cell body in the dorsal root ganglion
- for years
3- Reactivation
- viruses move down spinal nerve at a later time (shingles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diagnosis HHV3

A

1) Varicella/Chickenpox is diagnosed from teh characterisatic lesions
2) Shingel lesions can be more difficult to diagnose

17
Q

Treatment of HHV3

A

1) is usually self limiting
2) Management of symptoms ( anti-histamines)
3) Acyclovir

18
Q

Prevention of HHV3

A

1) Difficult to prevent exposure, since virus is shed before obvious signs appear
2) Vaccines against chickepox and shingles are available

19
Q

Talk about HHV-4

A

jkjk

20
Q

Characteristics of HHV-4

A

Genus Leymphocryptovirus

HHV ( Epstein-Barr Virus -EBV)

21
Q

Infections of HHV4

A

1- Burkitt’s Lymphoma
- malignant B cell lymphoma of the jaw and face, in african boys. M. Epstein and Y. Barr isolated EBV from lesions. The first virus causing cancer
2) Nasopharyngeal cancer (China):
genetic and envirpnmental factors
3) Infectious mononucleosis: Enlarged B lymphocytes, lobed nuclei
4) Implicated (not proven) in : chronic fatigue syndrome, oral leukoplakia (precancerous) in AIDS patients, Hodgkin’s Lymphoma

22
Q

Diseases associated with HHV4

A 
The immune response (age-dependent) conditions EBV-associated diseases:
1- Oral hairy leukoplakia: AIDs
2- Burkitt's Lymphoma: Malaria
3- Asymptomatic: Children
4- Infectious mononuceosis: Adulthood
23
Q

Epidemiology and pathogenesis of HHV-4 (EBV infections)

A

1- Transmission occurs via saliva
2- Binds C3d receptor = CR2 or CD21 on epithelial cells of pharynx and B cells
3- Initially infect epithelium of pharynx and parotid salivary glands ( cell lysis, budding)
4- Virus enters bloodstream and invades B lymphocytes
+ Become latent and suppresses apoptosis of B cells immortalizing them
+ EBV persists in memory B cells for lifetime, can be reactivated
5- Immune response csauses infectious mononucleosis symptoms
- Cytotoxic T cells kill virus-infected B lymphocytes: sore throatt, fever, enlargement of lymoh nodes, spleen and liver, fatigue
6- Infection in adults produces more serioous signs and symptoms
7- Cancer developement appears to depend on various cofactors:
sex, age, malaria fro Burkitt’s lymphoma, food , environment for nasopharyngeal cancer
8- Extreme diseases arise in individuals with T cell deficiency: infected B cells are not removed ( AIDS, immunosuppressed patients, elderly, malnourished children)

24
Q

Diagnosis of HHV4

A

1- Large, lobed B lymphocytes with atypical nuclei and neutropenia
2- Lymphocytosis (mononucleosis): activation and proliferation of T lymphocytes by infected B cells, atypical lymphocytes
3- Some diseases diagnosed by their characteristic signs
4- Serological tests: a high percentage ( 70 %) of adults have antibodies against EBV

25
Q

Treatment of HHV4

A

1- Burkitt’s lymphoma and Hodgkin’s Lymphoma respond well to chemotheraphy
2- Mononucleosis patients are treated to relievev the symptoms
3- Other conditions have no effective treatment

26
Q

Prevention of HHV4

A

1- Hard because virus is widespread and transmitted by saliva

27
Q

Talk about HHV5

A

jkjk

28
Q

Infections of HHV5

A

1- Infected cells become enlarged
2- One o fthe more common infections of humans
+50 % or more of the adult population in the US or EU is infected
+ 100% of the population of some developing countries test positive for antibodies against CMV
+ The most common virsal cause of Congenital defects
+CMV is a sexually transmitted disease
+ HHV-5 remains latent invarious cells for life

29
Q

Characteristics of HHV5

A

Cytomegalovirus

30
Q

Epidemiology and pathogenesis of HHV5

A

1) Transmission occurs through bodily secretions: Saliva, mucus, milk , urine, feces, semen, cervial secretions
+ Requires close contact and a large exchange of secretion
+ Usually occurs via sexual intercourse
+ Also transmittedf by in utero exposure ( mother with primary CMV infection during pregnancy, or virus ascenduing from the cervix after a recurrence), vaginal birth, blood transfusion, and organ transplants (kidney)
+ CMV infects 7.5 % of all neonates.
2) Most CMV infectio are asymptomatic
3) Opportunistic disorder: complications in fetuses, newborns, and immunodeficinet patients
+ Newborns may develop signs of infection (enlarged liver, and spleen, jaundice, anemia) Teratogenic: mental retardation, hearing and visual damage, death.
+ AID patients or immunosppressed adults may develop pneumonia, blindness, or cytomegalovirus mononucleosis. CMV diseases result from initial infections or latent viruses.

31
Q

Diagnosis of HHV5

A

1) Histology: detection of enlarged cells and cellular inclusions
owl’s eyes cell: diagnostic for CMV infection. Abnormally enlarged, enlargeed nuclei, basophilic intranuclear inclusion bodies which aere sites of viral assembly.

32
Q

Treatment of HHV5

A

1) Treatment of fetuses and newborns is difficult
+ Damage usually occurs before infection is discovered
+ Interferon, gammaglobulins
+Fomivirsen ( CMV complementray RNA) is used to treat CMV eyeinfections

33
Q

Prevention of HHV5

A

1- Condoms can reduce chances of infection

2- Organs for transplantation are screened or treated with mAbs anti-CMV

34
Q

Ineterleukin-1 receptor 8 (IL-1R8) plays a crucial role in NK cel differentiation and function

A

Regulatory functions of TIR8 in pathology
1- Pulmonary TB and P.Aeruginos infection
2- Fungal infection
3- Allergy and asth,a
4- Autoimmunity (EAE)
5- Intestinal inflammation Colitis - associated cancer
6- Brain inflammation
7- Chronic Lymphocytic leukemia
8- Arthritis
9- Kidney transplantation

M-CSF induces the expression of a membrane-bound form of IL-18 in a subset of human monocytes differentiating in vitro towards macrophages

IL-1R8 deficiency is associated with higher IFN-Y production and cytotoxic potential

IL-1R8 is associated with a more efficient MCMV control in liver

IL-1R8-deficient NKcells displayed enhanced effector functions upon infection

35
Q

Talk about HHV6

A

jkjkk

36
Q

Characteristics of HHV6

A

Human Herpesvirus 6
In the genus Roseolovirus
+ Universal endemic infection of children (6 months -2 years) almost 100% of the population has antibodies anti HHV-6

37
Q

Mode of transmission

A

1) Transmitted with respiratory droplets, via conjunctiva, nose, pharynx
+HHV-6
2) HHv 6 infects lymphocytes (CD4+ t cells_ and monocytes establishing latent infection
+ Causes ROSEOLA or EXANTHEM SUBITUM ( without malattia)
-abrupt fever, pink rash, resolved T-cel mediated immunity , but lifelong latent infection of T cells.
- can cause mononucleosis-like symptoms

38
Q

Talk about HHSV7

A

1) Roseolovirus

2) Orphan virus: not associated with disease. isolated from AIDS patient

39
Q

Talk about HHV8

A

1) Rhadinovirus
2) Causes Kaposi’s Sarcoma
- Cancer often seen in AIDs patients. Endothelial cells
- Lesions occur in oral cavity or skin. Nodules are highly infiltrated by inflammatory cells and associated with angiogenesis-lymphangiogenesis
- Virus is latent in B Lymphocytes and monnocytes
- The virus codes for proteins similae to IL-6, BCL-2, chemokines and chemokine receptors.
MOst common cancer in sub-saharan africa

Microbiology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions