Lecture 4 Flashcards
Paramyxovirus causes what major diseases
Mumps + Measles
HN (hemagglutinin-neuraminidase) associate with
Mumps
H (hemagglutinin) – binds surface receptors, no N
associate with
Measles
Togaviruses properties
Enveloped virus
Icosahedral capsid
ssRNA(+) virus
2 glycoprotein spikes – E1 and E2
Replicates in cytoplasm
Infects upper respiratory tract
Spread via viremia to lymphoid tissue, skin and other organs
Causes Rubella (also known as German measles)
Mumps virus
Highly contagious, lytic infection
Spread by viremia
2◦ infection of parotid gland; characterized by painful swelling
CNS infection in 50% of patients
Measles Virus
Highly contagious
Primary infection in epithelial cells
Secondary infection in lymphocytes & monocytes
Spread systemically through lymphatic system
Rash due to T cells targeting skin blood vessel endothelial cells
Enteroviruses contain
Poliovirus
Coxsackie A virus
Coxsackie B virus
Echovirus
Enterovirus
enteroviruses properties
no envelope
icosahedral capsid
small, ssRNA (+) viruses
linear mRNA genome
replicated & assembled in the cytoplasm
large family of viruses
very resistant to harsh conditions
enteroviruses (tolerate wide pH range)
transmitted by fecal-oral route
Lytic virus with specific tissue tropism
Enterovirus time course
6-12 days
*rash, ferbrile illness
T/F: Enteroviruses can survive harsh environments
TRUE
HERPESVIRUSES: PROPERTIES
Viral-glycoprotein rich envelope
Icosadeltahedral capsid
dsDNA viruses
Linear genome
3 subfamilies
Based on gene structure, site of latent infection
Replicated & assembled in the nucleus
Common infection, usually benign and asymptomatic but can be serious especially in immunocompromised individuals
Significant morbidity in eye, brain & disseminated infections
Some herpesviruses have highly specific tissue tropism
Released by lysis, exocytosis or cell-cell bridges
3 subfamilies of herpesviruses are
Alpha
Herpes simplex type 1 (HSV-1)
Herpes simplex type 2 (HSV-2)
Varicella-Zoster virus (VZV) – HHV-3
Beta
Cytomegalovirus (CMV) – HHV-4
Human Herpesvirus 6 & HHV-7
Gamma
Epstein-Barr Virus (EBV) – HHV-5
Kaposi’s Sarcoma-related Virus (HHV-8)
Herpes Virus life cycle slide 32 ig know it
Herpes simplex viruses
HSV-1 & HSV-2 (alphaherpesvirinae)
Genome encodes ~80 proteins
2 main groups
Viral replication
Viral DNA polymerase
Scavenging enzymes (create deoxyribonucleotides)
Other proteins
Attachment glycoproteins
Immune escape proteins
HSV infections properties
Lytic – fibroblasts & epithelial cells
Latent – non-dividing cells (neurons)
Non-permissive cells
Early & late genes not expressed
latency-associated transcripts (LATs)
micro-RNAs that inhibit gene expression
Persist in sensory neurons (ex. trigeminal neurons)
Avoid host immune response, asymptomatic
Block TAP, express Fc & complement receptors
Reactivation
Systemic infection, fever, stress, sun exposure
HSV-1 syndromes
Mucocutaneous lesions (cold sore, fever blister)
Pharyngitis
Eczema herpeticum
Encephalitis
HSV-2 syndromes
Genital herpes (sacral ganglion)
Neonatal HSV (often fatal – cell-mediated immunity not fully developed)
VARICELLA-ZOSTER VIRUS
VSV (Chicken pox virus) – HHV-3
Alphaherpesvirinae subfamily
Primary infection – chickenpox
Epithelial cells, fibroblasts, T cells
Recurrent infection – herpes zoster (shingles)
Neurons
Establishes a latent, recurrent, neuronal infection
Dorsal root or cranial nerve ganglia
Primary route of transmission – inhalation
Replicates in mucosal epithelium, cell-cell spread (synctium formation)
Spread by viremia to skin producing lesions (pox)
EPSTEIN-BARR VIRUS
EBV (gammaherpesvirinae subfamily) – HHV-4
3 infection outcomes:
Primary infection (productive, lytic)
Binds CR2 receptor expressed on selected epithelial cells and B cells (B cell parasite)
Early & late genes transcribed & translated
Latent infection in memory B cells – recurrence once B cell is activated (no early or late gene expression)
Immortalization of B cells
B cell lymphomas (African Burkitt lymphoma)
Nasopharyngeal carcinomas
EPSTEIN-BARR virus pt 2
Infectious mononucleosis (“kissing disease”)
Transmission through shedding virus
Proliferation & activation of B cells results in massive activation of T cells
T-cell-mediated immunity critical for controlling infection
Contributes to symptoms of infectious mononucleosis
lymphocytosis (increases in mononuclear cells)
swelling of lymph tissue
malaise
CYTOMEGALOVIRUS
CMV (betaherpesvirinae subfamily) – HHV-5
large genome, lots of proteins produced
dsDNA virus but harbors mRNA transcripts in capsid
Permissive cells
fibroblasts, epithelial cells, granulocytes, macrophages
Latent infection (non-permissive cells)
monocytes, lymphocytes, bone marrow stromal cells
Slow replication favors latent infections
Reactivated in immunocompromised individuals
Asymptomatic shedding of virus in body fluids
saliva, tears, urine, breast milk, semen
HERPESVIRUSES
HHV-6 (Roseola, herpes lymphotrophic virus)
nearly everyone seropositive by adulthood
replicates in salivary glands
high fever followed by neck & trunk rash
latent infection in lymphocytes (CD4+ T cells in particular) & monocytes
productive infection upon T cell activation
Herpes virus pt 2
HHV-8 (Kaposi Sarcoma-related virus)
similar to EBV (gammaherpesvirinae)
rare B cell lymphoma
Opportunistic infection in AIDS patients
HHV-8 proteins
IL-6 homologue – promotes growth
Bcl-2 analog – prevents apoptosis
