IndietroViruses: Structure, Replication, and Viral Diseases (Measles, Herpes)
Guida di studio - Note intelligenti
Appunti personalizzati basati sui tuoi materiali, ampliati con definizioni chiave, esempi e contesto.
Viruses: Introduction and Classification
Overview of Viruses, Viroids, and Prions
Viruses are acellular infectious agents that require host cells for replication. They are distinct from living organisms due to their inability to carry out independent metabolic processes.
Virion: The complete, infectious form of a virus outside a host cell, consisting of a nucleic acid core surrounded by a proteinaceous capsid.
Virus: Tiny acellular agent with either DNA or RNA as its genome; lacks cellular structure.
Prion: Infectious protein particle lacking nucleic acids; causes disease by inducing abnormal folding of normal proteins (e.g., Creutzfeldt-Jakob disease).
Viroid: Naked RNA molecule that infects plants; lacks a protein coat.
Are Viruses Alive?
Viruses are not considered living organisms because:
They are acellular (not made of cells).
Cannot reproduce independently.
Do not grow or undergo division.
Do not perform metabolism or synthesize proteins independently.
Structural Characteristics of Viruses
Basic Components
Nucleic Acid: Either DNA or RNA, single or double stranded.
Capsid: Protein coat made of subunits called capsomeres; provides protection and attachment to host cells.
Envelope: Some viruses have a lipid bilayer envelope derived from host cell membranes, containing viral glycoproteins.
Spikes: Protein projections from the capsid or envelope, involved in host cell recognition and attachment.
Virus Envelope
Acquired from host cell during replication or release.
Composed of phospholipids and viral proteins (glycoproteins).
Envelope proteins and glycoproteins are crucial for host recognition and penetration.
Virus Capsid Types
Helical Viruses: Hollow, cylindrical capsid (e.g., Rabies virus).
Polyhedral Viruses: Capsids with geometrical sides (e.g., Adenovirus).
Complex Viruses: Complicated structures, such as bacteriophages with additional components (e.g., tail fibers).
Enveloped Virus Structures
Envelope Helical Viruses: Helical capsid surrounded by an envelope.
Envelope Polyhedral Viruses: Polyhedral capsid surrounded by an envelope.
Virus Sizes
Viruses are much smaller than cells and organelles:
Poliovirus: ~30 nm
Bacteriophage T4: ~225 nm
Smallpox virus: ~200 nm x 300 nm
Red blood cell: ~10,000 nm diameter
Families of Viruses That Affect Humans
Classification by Genome Type
Genome Type | Viral Family | Important Genera |
|---|---|---|
Single-stranded DNA | Parvoviridae | Parvovirus |
Double-stranded DNA | Herpesviridae | Herpes simplex virus |
Single-stranded RNA (+) | Picornaviridae | Poliovirus, Rhinovirus |
Single-stranded RNA (-) | Orthomyxoviridae | Influenza virus |
Double-stranded RNA | Reoviridae | Rotavirus |
Retrovirus (ssRNA-RT) | Retroviridae | HIV |
Bacteriophage and Animal Viral Structure Compared
Host Specificity
Plant viruses infect plant cells.
Bacteriophages infect bacterial cells.
Animal viruses infect animal cells.
Animal Virus Replication
General Steps
Attachment: Virus binds specifically to host cell receptors via capsid proteins or envelope glycoproteins.
Penetration (Entry): Virus enters host cell by direct penetration, membrane fusion, or endocytosis.
Biosynthesis: Viral genome is replicated and viral proteins are synthesized using host cell machinery.
Assembly and Maturation: Viral components are assembled into new virions.
Release (Exit): New virions exit the cell by lysis, budding, or exocytosis.
Attachment
Specific interaction between viral proteins (spikes, capsomeres) and host cell receptors.
Determines host range and tissue tropism.
Penetration
Direct Penetration: Naked viruses inject genome into host cell.
Membrane Fusion: Enveloped viruses fuse with host membrane, releasing genome.
Endocytosis: Host cell engulfs virus in a vesicle; viral genome is released inside cell.
Biosynthesis
Viral nucleic acid and proteins are synthesized using host cell machinery.
Central Dogma: DNA → mRNA → Protein
Key equations:
Examples of Biosynthesis
Positive-sense ssRNA virus: Genome acts as mRNA (e.g., Rhinovirus).
Negative-sense ssRNA virus: Requires RNA-dependent RNA polymerase to synthesize mRNA (e.g., Rabies virus).
Double-stranded RNA virus: Unwinds and transcribes mRNA from dsRNA (e.g., Rotavirus).
Assembly, Maturation, and Release
Lysis: Host cell bursts, releasing naked viruses.
Budding: Enveloped viruses acquire envelope as they exit host cell.
Exocytosis: Viruses are released in vesicles.
Virus Latency
Some animal viruses remain dormant in host cells (latency).
Viral DNA may integrate into host chromosome, becoming a permanent part (e.g., HIV, chickenpox, herpes).
RT-ssRNA Virus Replication Cycle
Retroviruses (e.g., HIV) copy their RNA to DNA via reverse transcriptase.
Viral DNA integrates into host genome, establishing latency.
Viral Diseases: Measles and Herpes
Measles Virus (Morbillivirus)
Etiology: Measles virus (ssRNA, helical capsid, enveloped)
Virulence Factors:
Hemagglutinin: attaches to host epithelial cell receptors
Fusion protein: causes host cells to fuse and form syncytia (giant cells)
Clinical Features:
Initial symptoms: sore throat, dry cough, headache, conjunctivitis, swollen lymph nodes, fever
Koplik's spots: oral lesions
Maculopapular rash: spreads from head to trunk and extremities
Transmission: Airborne droplets; virus enters via nose, mouth, or conjunctiva
Diagnosis: Clinical signs (rash, Koplik's spots)
Treatment: No specific antiviral; ribavirin may be used; antibiotics for secondary infections
Prevention: Live attenuated vaccine (MMR)
Epidemiology:
Highly contagious
Humans are the only host
Vaccination has reduced incidence; outbreaks occur in unvaccinated populations
Herpes Simplex Virus (HHV-1 and HHV-2)
Etiology: Human Herpes Viruses 1 and 2 (dsDNA, icosahedral capsid, enveloped)
Virulence Factors:
Envelope glycoproteins: adhesion and fusion, formation of syncytia
Inactivation of complement
Latent infection: continual shedding even without symptoms
Clinical Features:
Lips: herpes labialis (cold sores)
Fingers: herpes whitlow
Conjunctiva: ocular herpes
Genitals: herpes genitalis
Pathogenesis:
Initial infection: replication in epithelial cells, inflammation, cell death, vesicle formation
Latent infection: virus remains inactive in nerve cells, reactivates intermittently
Diagnosis: Presence of characteristic lesions
Prevention: Gloves for healthcare workers; avoid contact with lesions
Epidemiology:
HHV-1: usually acquired in childhood, often asymptomatic
HHV-2: acquired in adolescence/adulthood, often via sexual activity
Both can be transmitted between oral and genital mucosa
Herpes infections in adults are rarely life-threatening; neonatal infections can be fatal
Summary Table: Virus Replication Steps
Step | Description |
|---|---|
Attachment | Virus binds to specific host cell receptors |
Penetration | Virus enters host cell (direct, fusion, endocytosis) |
Biosynthesis | Viral genome and proteins are synthesized |
Assembly/Maturation | Viral components assembled into new virions |
Release | Virions exit cell (lysis, budding, exocytosis) |
Additional info:
Central Dogma of Molecular Biology is essential for understanding viral biosynthesis:
Syncytia formation allows viruses to evade immune detection by spreading directly between cells.
Vaccination remains the most effective method for preventing viral diseases such as measles.