18.5 micro lecture

Why do rhinovirus infections recur throughout life?

Because there are >100 serotypes, each with different VP1 capsid proteins, so antibodies against one strain do not protect against others.

What host receptor does rhinovirus use to enter cells?

ICAM-1 (intercellular adhesion molecule 1)

Why does rhinovirus mainly infect the upper respiratory tract?

It replicates best at 33°C, which matches the cooler nasal passages.

What causes rhinovirus symptoms like runny nose?

Release of histamine and bradykinin → increased vascular permeability and fluid leakage

What type of genome does influenza virus have?

Segmented, negative-sense RNA

What is the main difference between antigenic drift and shift?

• Drift = small mutations over time (seasonal flu)

• Shift = major reassortment of genome segments (pandemics)

How does antigenic shift occur?

Two different influenza viruses infect the same cell → RNA segments reassort → new viral strain

Why is antigenic shift dangerous?

Creates a virus with new hemagglutinin/neuraminidase, so humans have no preexisting immunity → pandemic

What cells does influenza destroy first?

Ciliated epithelial cells in respiratory tract

Why are secondary bacterial infections common after influenza?

Influenza damages lung epithelium and weakens immune defenses, allowing bacteria like Strep pneumoniae to infect.

What immune response causes flu symptoms (fever, aches)?

Viral activation of interferon signaling and inflammatory cytokines

What cells does HIV primarily infect?

CD4⁺ T helper cells

What receptors does HIV gp120 bind?

• CD4 receptor

• CCR5 chemokine receptor

Why is CCR5 binding important in HIV infection?

It allows viral entry and disrupts immune signaling between cells

What does HIV Nef protein do?

• Prevents apoptosis of infected T cells

• Helps infected cells survive longer for viral replication

What does HIV Tat protein do inside the cell?

Increases viral transcription AND is secreted to:

• Decrease MHC I expression

• Alter cytokines

• Trigger apoptosis in uninfected cells

What is the result of HIV infection on T cells over time?

Progressive loss of CD4⁺ T cells → immunodeficiency (AIDS)

Why are HIV patients vulnerable to infections?

Loss of CD4⁺ T cells → impaired adaptive immune response

What disease does HPV cause initially?

Warts (benign epithelial growths)

How does HPV cause cancer?

Viral protein E7 inactivates pRb → releases E2F → uncontrolled cell division

What is the normal role of pRb?

It blocks cell cycle progression by inhibiting E2F transcription factor

Why does HPV induce cell division?

More host cell division = more viral replication

What long-term disease can HPV cause?

Cervical and other epithelial cancers

What is viral latency?

Virus remains in host cells dormant with no active replication

Where does herpesvirus remain latent?

Sensory neurons

What triggers herpesvirus reactivation?

• Stress

• UV light

• Fever

• Immune suppression

What happens to herpesvirus DNA during latency?

It circularizes and remains silent in the nucleus

What are viral microRNAs used for in herpesvirus?

They inhibit apoptosis pathways so infected cells survive during reactivation

Why does herpesvirus avoid immune detection during latency?

It produces no viral proteins, so immune system cannot recognize infected cells

How do viruses reduce immune detection using MHC I?

They down-regulate MHC I expression, reducing antigen presentation

What is molecular mimicry in viruses?

Virus produces proteins that mimic host molecules to avoid immune detection (e.g., cytomegalovirus mimics MHC I)

Why is reduced MHC I dangerous for viruses?

It triggers NK cells—but some viruses evade NK cells using mimic proteins

How do viruses manipulate cytokines?

They alter inflammatory signaling to weaken immune response or reduce detection

Why does HIV cause immunodeficiency but influenza does not?

HIV destroys CD4⁺ T cells, while influenza only causes temporary respiratory infection.

Why can influenza cause pandemics but rhinovirus does not?

Influenza undergoes antigenic shift (major genome change); rhinovirus mainly has many stable serotypes.

What is the key difference between latency and active infection?

• Latency = no viral protein expression

• Active infection = full viral replication and protein production