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Infectious Disease Midterm > Lecture 4 > Flashcards

Lecture 4 Flashcards

help.

1
Q

Mumps, measles, and rubella

A

Mumps is a viral infection that causes fever, headache, muscle aches, loss of appetite, and swollen salivary glands. It can also cause complications such as meningitis, encephalitis, and infertility.

Measles is a viral infection that causes fever, cough, runny nose, red eyes, and a rash. It can also cause complications such as pneumonia, encephalitis, and death.

Rubella is a viral infection that causes fever, rash, swollen glands, and joint pain. It is usually mild in children, but it can cause serious birth defects if a pregnant woman contracts the virus.

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2
Q

(this is review)

A

section title

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3
Q

Envelope type

A

pleomorphic envelope

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4
Q

Capsid type

A

Helical nucleocapsid

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5
Q

Genome type

A

Linear

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6
Q

What type of proteins does it carry

A

nucelocapsid-associated proteins

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7
Q

How can you tell the genera apart?

A

Through the attachment proteins

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8
Q

Paramyxoviruses can cause what diseases?

A

Measles and mumps

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9
Q

How do Paramyxoviruses invade cells?

A

Through membrane fusion and then budding

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10
Q

Mumps attachment proteins

A

HN: Hemagglutinin-neuraminidase

which is responsible for virus attachment, interacts with the fusion protein in a virus type-specific manner to induce efficient membrane fusion.

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11
Q

Measles viral-attachment proteins

A

H: Hemagglutinin

It is responsible for binding the virus to the cell that is being infected.

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12
Q

Genera of Paramyxoviruses

A

Morbillivirus
Paramyxovirus
Pneumovirus

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13
Q

Morbillivirrs

A

Causes measles

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14
Q

Paramyxovirus

A

Mumps virus
Paraninfluenza

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15
Q

Pnuemovirus

A

RSV (respiratory syncytial virus)
Metapneumovirs

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16
Q

Paramyxoviruses Replication Scheme

A

Same as the other ssRNA (-) Schemes.

Make one positive and use it for viral proteins
Make one positive and then use it to make more negative strands that are used in packaging of the new viruses

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17
Q

NP (Nucleoprotein):

A

Function: Binds & protects viral RNA..

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18
Q

P (Polymerase Phosphoprotein):

A

function: Facilitates RNA replication.

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19
Q

L (RNA Polymerase):

A

Involved in RNA replication.

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20
Q

F Protein (Membrane Protein):

A

Promotes fusion & viral entry.

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21
Q

HN (Hemagglutinin-Neuraminidase):

A

Binds surface receptors and has neuraminidase activity.

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22
Q

H (Hemagglutinin):

A

Binds surface receptors.

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23
Q

M Protein (Matrix Protein):

A

Involved in the assembly of virions.

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24
Q

Enveloped or not? Togaviruses (rubella)

A

Enveloped

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25
Q

Capsid type Togaviruses (rubella)

A

Icosahedral Capsid

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26
Q

genome type. Togaviruses (rubella)

A

ssRNA (+) Capsid

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27
Q

Glycoprotein spikes

Togaviruses (rubella)

A

E1 & E2:

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28
Q

E1 Protein Function:

A

: The E1 protein in rubella virus is involved in the fusion of the viral envelope with the host cell membrane during the process of viral entry. This fusion allows the virus to enter the host cell.

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29
Q

E2 Protein:

A

The E2 protein in rubella virus is primarily responsible for the attachment of the virus to specific receptors on the surface of host cells. It binds to cellular receptors, facilitating the initial binding of the virus to the host cell.

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30
Q

Where do togaviruses replicate?

A

IN the cytoplasm

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31
Q

Where do togaviruses infect

A

Infects the upper respiratory tract

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32
Q

How are they spread

A

Through viremia to lymphoid tissue, skin and other organs

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33
Q

Main disease togaviruses cause

A

Rubella

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34
Q

Rubella replications cheme

A

ssRNA (+)

Same as always

One translated to protein and one translated to negative and then used to make more positive strands

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35
Q

Rubella virus structure

A

Check slide 11
Capsid Protein
Enveloped etc

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36
Q

Life cycle of Rubella Virus

A

The life cycle of rubella virus, like many other viruses, involves a series of steps that allow the virus to infect host cells, replicate, and spread. Here is an overview of the rubella virus life cycle:

  1. Attachment and Entry:
    • The initial step in the rubella virus life cycle is the attachment of the virus to specific receptors on the surface of host cells. In the case of rubella virus, the E2 protein plays a crucial role in this attachment.
    • Once attached to the host cell, the virus is internalized into the host cell through endocytosis, a process where the host cell membrane engulfs the virus particle.
  2. Uncoating:
    • After internalization, the viral envelope fuses with the host cell membrane, releasing the viral genome (single-stranded RNA) into the cytoplasm of the host cell.
  3. Translation and Replication:
    • The released viral RNA is then translated to produce viral proteins, including replication and structural proteins.
    • Viral RNA serves as a template for the replication of new viral RNA strands.
  4. Assembly:
    • New viral particles are assembled within the host cell. The structural proteins, including the E1 and E2 glycoproteins, are involved in forming the viral envelope.
    • The viral genome is encapsulated by the newly formed viral particles.
  5. Budding and Release:
    • The newly assembled rubella virus particles are transported to the cell surface.
    • The virus particles are released from the host cell by budding, a process where the viral envelope is acquired from the host cell membrane, and the mature virus particles are released into the extracellular environment.
  6. Infection of New Cells:
    • The released rubella virus particles can then infect neighboring host cells, repeating the cycle.
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37
Q

Mumps

A

Virus Type: Mumps Virus (Paramyxovirus)

Transmission Type: Respiratory droplets, close contact

Incubation Period: 12-25 days

Symptoms: Swelling of salivary glands (parotitis), fever, headache, muscle pain

Duration of Illness: 7-10 days

Rash: No typical rash

Severity: Generally mild, but complications can occur

Fetal Infection: Rare, but possible

Vaccine: Mumps component in MMR (Measles, Mumps, Rubella) vaccine

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38
Q

Measles

A

Virus Type: Measles Virus (Paramyxovirus)

Transmission Type: Airborne, highly contagious
Incubation Period: 7-14 days

Symptoms: High fever, cough, runny nose, red eyes, characteristic rash

Duration of Illness: About 7-10 days

Rash: Characteristic red, raised rash

Severity: Can be severe with complications, including pneumonia

Fetal Infection: Risk to pregnant women, especially in the first trimester

Vaccine: Measles component in MMR (Measles, Mumps, Rubella) vaccine

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39
Q

Rubella (German Measles)

A

Virus Type: Rubella Virus (Togavirus)

Transmission Type: Respiratory droplets, close contact

Incubation Period: 12-23 days

Symptoms: Mild rash, fever, swollen lymph nodes

Duration of Illness: About 3 days

Rash: Characteristic pink rash

Severity: Typically mild in children and adults, but can have complications, more severe in pregnant women

Fetal Infection: High risk of congenital rubella syndrome if a pregnant woman is infected
Vaccine: Rubella component in MMR (Measles, Mumps, Rubella) vaccine

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40
Q

Mumps Virus

A

Highly contagious lytic infection

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41
Q

How does mumps spread in the body?

A

Viremia

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42
Q

Where is the secondary infection for mumps?

A

Can spread to the parotid gland

Causes swelling in the neck

(google picture to remember)

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43
Q

Spread of Mumps in the body

A

Enters in the respiratory tract, replication, viremia, systemic infection, then to the parotid gland, the testes/ovaries/ eye/ear (etc) , the CNS, and the pancreas

Can lead to diabetes or swelling

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44
Q

Measles Virus

A

Highly contagious

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45
Q

Primary infection of measles

A

In the epithelial cells

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46
Q

Secondary infection

A

In lymphocytes and monocytes

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47
Q

How is measles spread through the body?

A

The lymphatic system

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48
Q

Characteristic symptom of measles

A

RASH!!!!

Happens because T cells will target the skin blood vessels and endothelial cells

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49
Q

Spread of Measles in the body

A

Inoculates the respiratory tract, replication, lymphatic spread, viremia, wide dessemination through the whole body, virus infected endothelium, RASH!!!, and then diff. outcomes

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50
Q

Picornaviruses

A

Picornaviruses are a family of small, non-enveloped RNA viruses that are responsible for a variety of diseases in humans and animals. They are known for their simple, single-stranded RNA genomes and their ability to cause a wide range of illnesses. Here are some key points about picornaviruses:

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51
Q

Enteroviruses

A

Enteroviruses are a group of viruses that belong to the Picornaviridae family. They are named “enteroviruses” because they typically enter the body through the gastrointestinal tract.

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52
Q

Types of Picornaviruses

A

Poliovirus - Poliomyelitis (polio)
Coxsackievirus - Hand, foot, and mouth disease, herpangina, myocarditis, viral meningitis
Echovirus - Aseptic meningitis, respiratory illnesses, febrile illnesses
Rhinovirus - Common cold
Enterovirus - Various respiratory and gastrointestinal infections, as well as more serious conditions
Hepatitis A Virus - Hepatitis A
Cardiovirus - Encephalomyocarditis virus (primarily infects rodents)

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53
Q

Enterovirsues

A

Poliovirus
Coxsackie A virus
Coxsackie B virus
Echovirus
Enterovirus

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54
Q

Rhinovirus

A

Common cold

Under the umbrella of picornaviruses

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55
Q

Cardiovirus

A

Encephalomyocarditis virus (EMCV).

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56
Q

Apthovirus

A

Aphthoviruses belong to the family Picornaviridae and are responsible for causing foot-and-mouth disease (FMD) in cloven-hoofed animals, such as cattle, pigs, sheep, and goats.

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57
Q

Hepatovirus

A

Hepatitis A

Under the picornaviruses umbrella

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58
Q

Poliovirus time course

A

4-35 days

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59
Q

Coxsackievirus time course

A

2-10 days

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60
Q

Echovirus

A

2-14 days
Meningitis

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61
Q

Entervirus

A

6-12 days
Causes rash, and febrile illness

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62
Q

Do enteroviruses have an envelope?

A

No envelope

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63
Q

Capsid shape of enteroviruses

A

Icosahedral capsid

64
Q

Genome type: enteroviruses

A

Small ssRNA (+) viruses

65
Q

What’s special about enteroviruses genome?

A

it is linear mRNA genome.

One of the unique features of enteroviruses is that their genome resembles messenger RNA (mRNA), and this characteristic allows for the efficient translation of viral proteins.

66
Q

Where are enteroviruses replicated & assembled?

A

The cytoplasm

67
Q

How resistant to diseases are enteroviruses?

A

Very resistant!
Enteroviruses can tolerate alot of pH range & this is why they’re GI tract viruses

67
Q

how are enterviruses transmitted?

A

Fecal-oral route

68
Q

Lytic/Non-lyitc?

enteroviruses

A

Lytic viruses w/ specific tissue tropism

69
Q

Enteroviruses: Life cycle

A

Attachment and Entry:

Enteroviruses initially attach to specific receptors on the surface of host cells. Poliovirus, for example, attaches to the poliovirus receptor (CD155) on host cells.
After attachment, the virus enters the host cell through endocytosis.

Uncoating:
Once inside the host cell, the viral capsid is disassembled, and the viral RNA genome is released into the cytoplasm.

Translation and Replication:
The enterovirus genome, which resembles mRNA, is directly translated by host cell ribosomes to produce a single polyprotein.
This polyprotein is then cleaved into individual viral proteins by viral proteases.

Replication of the viral RNA occurs, leading to the synthesis of more viral RNA.

Assembly:

New viral particles are assembled in the cytoplasm, and the viral RNA is encapsidated by structural proteins.

Budding and Release:
The newly formed virus particles are released from the host cell through a process that does not typically involve lysis but rather the extrusion of virus particles.

Infection of New Cells:
The released enterovirus particles can infect neighboring host cells and repeat the replication cycle.

70
Q

Primary viremia of enteroviruses?

A

Blood

71
Q

Secondary viremia of enteroviruses

A

Target tissues and organs
- includes skin, muscle, brain, meninges, liver

72
Q

Diseases of enterviruses

A

Common Cold
Hand, Foot, and Mouth Disease (HFMD)
Aseptic Meningitis
Myocarditis
Pericarditis
Acute Hemorrhagic Conjunctivitis (AHC)

73
Q

How are enteroviruses transmitted?

A

through human fecal matter, sewage, solid waste, landfills, etc.

Can survive harsh environments

Cause fever and rash

74
Q

Herpes Viruses

A

Herpesviruses are a family of DNA viruses known for their ability to establish latent infections and cause a wide range of diseases in humans and animals. There are eight known human herpesviruses, and each is associated with specific clinical conditions

75
Q

Do herpres viruses have an envelope?

A

Yes very much so

Viral-glycorprotien rich envelope

76
Q

Capsid Type: Herpes

A

Icosadeltahedral capsid

77
Q

Virus type? Herpes

A

dsDNA virus

78
Q

Genome type: Herpes

A

Linear genome

79
Q

What’s used to classify herpesvirus

A

Site of latent infection & gene structure

80
Q

Where are herepes replicated and assembled?

A

In the nucleus

81
Q

How common are herpes infections?

A

Pretty common

can be asymptotic and benign for the avg person but theymight be serious in immunocompromised individuals

82
Q

Morbidity of herepes ?

A

Can be morbid in the eye, brain or in disseminated infections

83
Q

Do herepes have specific tropism?

A

Yes some can have highly specific tropism

84
Q

How are they released from the host cell? Herpes

A

Through lysis, exocytosis & cell-cell bridges

85
Q

There are 3 subfamilies of Herpes viruses. What are they?

A

Alpha
Beta
Gamma

86
Q

Alpha Herpesvirus

A

HERPES SIMPLEX HSV1
HERPES SIMPLEX 2 HSV2
VARICELLA-ZOSTER VIRUS HHV 3

87
Q

Beta

A

Cytomegalovirus -HHV
Human Herpesvirus 6 & HHV7

88
Q

Gamma

A

Epstien-bar virus EBV : HHV5
Kaposis’s sarcoma-related virus HHV 8

89
Q

Herpes Replication scheme

A

dsDNA virus

Converts to MRNA which is then translated to viral proteins

dsDNA is copied and then used in new viruses

90
Q

Herpes Time Course

A

(refer to the chart)

91
Q

Herpes Viruses Structure

A

(kinda looks like the Bengali flag)

92
Q

HerpesViruses: Life Cycle

A

The virus enters the host cell, delivering its double-stranded linear DNA genome.

93
Q

Circularization of the Genome:

A

Once inside the host cell, the viral DNA circulates with “sticky ends,” which means the ends of the linear DNA strands can base-pair with each other.

This circularization process transforms the linear DNA into a circular chromosome that can serve as a template for replication and transcription.

94
Q

Gene Expression and Transcription

A

The circularized viral DNA contains genes that encode various viral proteins and enzymes.

Early genes are transcribed first, leading to the synthesis of specific viral proteins.
One of these early gene products is the viral DNA polymerase, which is an enzyme responsible for replicating the viral genome.

95
Q

Concatemeric DNA Formation:

A

During the replication process, the viral DNA polymerase synthesizes new DNA strands.

Instead of producing individual genome-length DNA molecules, the DNA polymerase creates a long chain of repeated viral genomes, known as a “concatemeric DNA.”

The concatemeric DNA can be very long, containing 20 to 30 or more genome-length copies in a single strand.

96
Q

Herpes Simplex Virus 1 (HSV-1):

A

Diseases: Oral herpes (cold sores), herpes labialis, herpetic gingivostomatitis, and can cause genital herpes.

97
Q

Herpes Simplex Virus 2 (HSV-2):

A

Diseases: Genital herpes and can also cause oral herpes.

98
Q

HHV3:

Varicella-Zoster Virus (VZV):

A

Diseases: Chickenpox (varicella) and shingles (herpes zoster).

99
Q

Epstein-Barr Virus (EBV):

A

Infectious mononucleosis (mono), Burkitt’s lymphoma, nasopharyngeal carcinoma, and other lymphoproliferative disorders.

100
Q

Cytomegalovirus (CMV):

A

Cytomegalovirus infection, which can be asymptomatic or cause symptoms, particularly in immunocompromised individuals.

101
Q

Human Herpesvirus 6 (HHV-6):

A

Roseola infantum (exanthema subitum), a childhood illness with high fever and a characteristic rash.

102
Q

Human Herpesvirus 7 (HHV-7):

A

Causes roseola, but its role in disease is less well-understood compared to HHV-6.

103
Q

Kaposi’s Sarcoma-Associated Herpesvirus (KSHV) or Human Herpesvirus 8 (HHV-8):

A

: Kaposi’s sarcoma, primary effusion lymphoma, multicentric Castleman disease, and other conditions primarily seen in immunosuppressed individuals, especially those with HIV/AIDS.

104
Q

HSV-1 & HSV-2

A

HSV-1 and HSV-2 genomes encode approximately 80 proteins.

These viruses belong to the Alphaherpesvirinae subfamily.

105
Q

Viral Replication:

A

Both HSV-1 and HSV-2 follow a similar pattern of viral replication within host cells.

Viral DNA Polymerase:

These herpesviruses encode a viral DNA polymerase, which is crucial for replicating their DNA genomes.

106
Q

Scavenging Enzymes:

A

HSV-1 and HSV-2 produce scavenging enzymes that create deoxyribonucleotides, essential building blocks for DNA replication.

107
Q

Attachment Glycoproteins:

A

These viruses possess attachment glycoproteins that facilitate their entry into host cells.

108
Q

Immune Escape Proteins:

A

HSV-1 and HSV-2 have immune escape proteins that help them evade the host’s immune system.

109
Q

Lytic Phase: HSV 1 /2

A

HSV-1 & HSV-2 infect fibroblasts and epithelial cells during the lytic phase.

110
Q

Latent phase: HSV1/2

A

During latency, herpesviruses persist in non-dividing cells, primarily neurons.

In non-permissive cells, early and late genes are not expressed.

111
Q

Latency-Associated Transcripts (LATs):

A

LATs are non-coding RNAs produced during latency, aiding in immune evasion.

112
Q

Micro-RNAs:

A

Micro-RNAs produced during latency inhibit gene expression

113
Q

Sensory Neurons:

A

Herpesviruses persist in sensory neurons, such as trigeminal neurons.

This latency helps the virus avoid the host’s immune response, often causing no symptoms.

114
Q

Immune Evasion:

A

Herpesviruses block the Transporter Associated with Antigen Processing (TAP).

They express Fc and complement receptors.

This helps the virus evade immune detection.

115
Q

Reactivation:

A

Reactivation from latency can occur due to systemic infection, fever, stress, or sun exposure.

It leads to recurrent symptoms or outbreaks.

116
Q

HSV 1 INFECTION & LATENCY:

A

HSV infects the host and will establish LATENCY in the trigeminal ganglia.

This is how the virus will remain in the body time and time again

During latency, the virus remains dormant within nerve cells.

Periodically, the virus can reactivate, leading to the appearance of a cold sore on the lips or around the mouth.

117
Q

Clinical Manifestations of HSV 1

A

Cold sores, fever blisters, Pharyngitis, Encephalitis

118
Q

HSV 2

A

Genital Herpes
neonatal HSV- can be fatal to babies when immunity is not developed

119
Q

VZV (Varicella-Zoster Virus) - HHV-3

A

Primary Infection - Chickenpox:

Targets epithelial cells, fibroblasts, and T cells.
‘
Characterized by a widespread rash, fever, and itching.

120
Q

HHV3:
Virus family

A

Virus Family: Alphaherpesvirinae subfamily

121
Q

Recurrent Infection -

A

Will become Herpes Zoster (Shingles):

Occurs in neurons, particularly the dorsal root or cranial nerve ganglia.

122
Q

Primary Route of Transmission: HHV3

A

Contracted through inhalation of respiratory droplets containing the virus.

123
Q

Where does HHV 3 replicate?

A

VZV undergoes replication in mucosal epithelial cells during the primary infection. This replication leads to the formation of new virus particles.

124
Q

How is HHV3 Spread in the body?

A

Viermia:

VZV can spread systemically via viremia, a condition in which the virus enters the bloodstream. As the virus circulates in the bloodstream, it can reach the skin, leading to the development of characteristic skin lesions. These skin lesions are often described as “pox” and are a hallmark of chickenpox, the primary infection caused by VZV.

125
Q

VZV virus mechanism

A

Droplets: Infection often begins with the inhalation of respiratory droplets containing the virus.

Respiratory Tract: The virus initially infects the respiratory tract.

Lymphatics: It can enter the lymphatic system, allowing it to travel through the body.

Liver/Spleen: In some cases, the virus may reach the liver and spleen.

Viremia: The virus can spread systemically through viremia, entering the bloodstream.

Membranes and Skin:

As it circulates in the bloodstream, the virus can reach mucous membranes and the skin, leading to the characteristic skin lesions seen in certain infections.

Latent in Neurons: After the primary infection, the virus establishes latency in neurons, where it remains dormant for an extended period.

126
Q

EBV (Epstein-Barr Virus) - HHV-4

A

virus Subfamily: Gammaherpesvirinae

127
Q

Primary Infection of EBV

A

During primary infection, EBV replicates actively, leading to lytic infection.

Binds to CR2 receptor expressed on selected epithelial cells and B cells.

Early & Late genes are transcribed & translated

128
Q

Latent Infection in Memory B Cells:

A

Following the primary infection, EBV establishes latent infection in memory B cells.

During latency, there’s no active viral replication (no early or late gene expression).

Recurrence can occur when the B cell is activated, leading to virus reactivation.

129
Q

Immortalization of B Cells:

A

EBV has the ability to immortalize B cells, preventing their natural cell death.

This contributes to the development of B cell lymphomas, such as African Burkitt lymphoma.

or Nasopharyngeal carcinomas

Forcing the B cells to continue replicating

130
Q

Infectious mononucleosis (“kissing disease”)

A

Typically transmitted through the shedding of the virus, often through the exchange of saliva, giving it the nickname “kissing disease.”

131
Q

Proliferation of B/T cells: EBV

A

EBV infection leads to the proliferation and activation of B cells, resulting in a massive activation of T cells.

132
Q

T-Cell-Mediated Immunity

EBV

A

T-cell-mediated immunity plays a critical role in controlling the EBV infection but also contributes to the symptoms of infectious mononucleosis.

133
Q

Symptoms of EBV

A

Lymphocytosis: Characterized by an increase in mononuclear cells in the blood.

Swelling of lymphatic tissue, especially the lymph nodes.
Malaise and a general feeling of unwellness are common symptoms.

134
Q

EBV Mechanism

A

EBV in saliva -> B cells/epithelial cells of oropharynx -> B cell proliferation -> activates T cells and can lead to latency or malaise.

B cells in the oropharynx can cause shedding in saliva and pharyngitis

135
Q

Clinical Syndrome of ESV

A

Symptoms:
Fatigue
Severe sore throat
High fever
Swollen lymph nodes
Enlarged spleen (potential danger)
Swollen liver
Headaches
Rash (less common)
Muscle aches
Loss of appetite

136
Q

CMV (Cytomegalovirus) - HHV-5:

A

Member of the betaherpesvirinae subfamily

137
Q

Permissive cells that allow HHV5 to replicate

A

Permissive cells: Fibroblasts, epithelial cells, granulocytes, macrophages.

137
Q

Latent infection (non-permissive cells)

A

monocytes, lymphocytes, bone marrow stromal cells

Slow replication favors latent infections

138
Q

Reactivation in immunocompromised individuals of HHV 5

A

Can be reactivated in immunocompromised individuals, leading to active infection.

139
Q

Asymptomatic shedding of HHv5

A

Asymptomatic Shedding:
Virus can be shed in various body fluids without causing symptoms.
Body fluids include saliva, tears, urine, breast milk, and semen.

140
Q

CMV: normal infection

A

Can cause an asymptomatic carrier or mono

141
Q

CMV: in a neonate

A

Cytomegalic inclusion disease

142
Q

CMV in an immunocompromised individual

A

Multisite symptomatic disease

143
Q

HHV6

A

(Roseola, Herpes Lymphotrophic Virus):

144
Q

Prevalence: HHV6

A

Nearly everyone is seropositive (has antibodies) to HHV-6 by adulthood.

145
Q

Replication: HHV6

A

Replicates in the salivary glands.

146
Q

Clinical Presentation: HHV6

A

Typically presents with high fever followed by a rash on the neck and trunk.

147
Q

Latent Infection HHV6

A

Virus establishes latent infection in lymphocytes, particularly CD4+ T cells and monocytes.

148
Q

Productive Infection: HHV6

A

Reactivates and produces active infection upon T cell activation.

149
Q

HHV6 REACTION MECHANISM

A

HHV 6 -> incubation -> fever -> no fever & rash appears -> recovery

150
Q

HHV-8 (Kaposi Sarcoma-related virus):

A

Classification:
Similar to EBV (Epstein-Barr virus), belongs to the gammaherpesvirinae subfamily.

151
Q

Clinical Association:

A

Associated with rare B cell lymphoma.

Causes opportunistic infections, especially in AIDS patients.

152
Q

HHV-8 Proteins:

A

Produces specific proteins with notable functions:

IL-6 homologue

Bcl-2 analog

153
Q

IL-6 homologue function

A

Promotes cell growth.

154
Q

Bcl-2 analog

A

Prevents programmed cell death (apoptosis).

Infectious Disease Midterm (5 decks)

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