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 and are classified alongside viroids and prions, which are also infectious but differ in structure and replication mechanisms.

• 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 containing either DNA or RNA as its genome; lacks cellular structure.

• Viroid: Naked RNA molecule that infects plants; does not encode proteins.

• Prion: Proteinaceous infectious particle lacking nucleic acids; replicates by converting normal proteins into abnormal prion forms.

Are Viruses Alive? Viruses are not living organisms because they:

• Are acellular (not made of cells)

• Cannot reproduce independently

• Do not grow or undergo division

• Do not perform metabolism

• Cannot synthesize proteins on their own

Structural Characteristics of Viruses

Basic Components

Viruses are composed of nucleic acid (DNA or RNA), proteins, and sometimes a lipid envelope derived from the host cell membrane.

• Nucleic Acid: The genetic material, either DNA or RNA, single or double stranded.

• Capsid: Protein coat made of subunits called capsomeres; provides protection and attachment to host cells.

• Envelope: Lipid membrane acquired from host cell during replication or release; contains viral glycoproteins and spikes for host recognition.

• Spikes: Protein projections from the capsid or envelope, important for host cell attachment.

Formula:

Capsid Types

• Helical Viruses: Hollow, cylindrical capsid (e.g., Ebola virus).

• Polyhedral Viruses: Capsids with geometrical sides (e.g., Adenovirus).

• Complex Viruses: Complicated structures, such as bacteriophages with additional components (e.g., T4 phage).

Envelope Structure

• Acquired from host cell membrane during viral replication or release.

• Composed of phospholipids and viral proteins (glycoproteins).

• Envelope proteins and glycoproteins are crucial for host cell recognition and penetration.

Virus Sizes

Viruses are much smaller than cells, typically ranging from 20 nm to 300 nm in diameter. For comparison:

• Red blood cell: ~10,000 nm

• E. coli bacterium: ~1,000 x 3,000 nm

• Poliovirus: ~30 nm

• Bacteriophage T4: ~50 x 225 nm

• Smallpox virus: ~200 x 300 nm

Families of Viruses That Affect Humans

Classification by Genome Type

Viruses are classified based on their nucleic acid type and structure. Major families include:

Additional info: Table entries inferred from standard virology classification.

Bacteriophage and Animal Viral Structure Compared

Host Specificity

Viruses are highly specific to their host organisms:

• Plant viruses infect plant cells

• Bacteriophages infect bacterial cells

• Animal viruses infect animal cells

Bacteriophages often have complex structures with a head, tail, and tail fibers, while animal viruses may be helical, polyhedral, or enveloped.

Animal Virus Replication

General Replication Cycle

Animal viruses replicate through a series of steps:

1. Attachment: Virus binds specifically to host cell receptors via capsid proteins or envelope glycoproteins.

2. Penetration (Entry): Virus enters the host cell by direct penetration, membrane fusion, or endocytosis.

3. Biosynthesis: Viral genome is replicated and viral proteins are synthesized using host cell machinery.

4. Assembly and Maturation: Viral components are assembled into new virions.

5. 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 their genome into the host cell.

• Membrane fusion: Enveloped viruses fuse with host cell membrane, releasing genome.

• Endocytosis: Virus is engulfed by host cell and uncoated inside the cytoplasm.

Biosynthesis

Viral nucleic acid and proteins are synthesized using host cell machinery. The process follows the central dogma:

• DNA is transcribed to mRNA in the nucleus.

• mRNA is translated to protein in the cytoplasm.

Formula:

Assembly, Maturation, and Release

• Lysis: Host cell bursts, releasing naked viruses.

• Budding: Enveloped viruses acquire their envelope as they exit the cell.

• Exocytosis: Viruses are released in vesicles.

Virus Latency

• Some animal viruses remain dormant in host cells (latency).

• Latent viral DNA may integrate into host chromosome (e.g., HIV, herpesvirus).

• Latent infections can reactivate, causing recurrent disease.

RT-ssRNA Virus Replication Cycle

Retroviruses (e.g., HIV) copy their RNA genome into DNA using reverse transcriptase. The DNA integrates into the host genome, establishing latency.

• HIV is a single-stranded RNA virus with a capsid and envelope.

• Reverse transcription:

• Integration into host chromosome by integrase.

Viral Diseases: Measles and Herpes

Measles Virus (Morbillivirus)

Measles is a highly contagious viral disease affecting the skin and respiratory system.

• Etiology: Measles virus (Morbillivirus), ssRNA (-), helical capsid, enveloped.

• Virulence Factors:

  • Hemagglutinin: Attaches to host epithelial cell receptors.

  • Fusion protein: Fuses host cells, forming syncytia (giant cells).

• Clinical Features:

  • Initial symptoms: sore throat, dry cough, headache, conjunctivitis, swollen lymph nodes, fever.

  • Characteristic oral lesions: Koplik's spots.

  • Maculopapular rash spreads from head to trunk and extremities.

• Transmission: Airborne droplets; virus enters via nose, mouth, or conjunctiva.

• Diagnosis: Clinical signs (Koplik's spots, rash).

• Treatment: No specific antiviral; ribavirin may be used; antibiotics for secondary bacterial infections.

• Prevention: Live attenuated vaccine (MMR).

• Distinguishing Features: Maculopapular rash; secondary bacterial ear and sinus infections common.

• Epidemiology:

  • Highly contagious; humans are the only host.

  • Vaccination has reduced incidence; eradicated in USA in early 2000s but has re-emerged.

Herpes Simplex Virus (HHV-1 and HHV-2)

Herpes simplex viruses cause recurrent skin and mucous membrane infections.

• Etiology: Human Herpes Virus 1 and 2 (HHV-1, HHV-2); dsDNA, icosahedral capsid, enveloped.

• Virulence Factors:

  • Envelope glycoproteins for adhesion and fusion.

  • Formation of syncytia; inactivation of complement.

  • Latent infection with continual low-level shedding.

• Clinical Features:

  • Lips: herpes labialis (cold sores)

  • Fingers: herpes whitlow

  • Conjunctiva: ocular herpes

  • Genitals: herpes genitalis

• Pathogenesis:

  • Initial replication in epithelial cells, causing inflammation and cell death.

  • Blisters (vesicles) form, filled with virions; break to release virus.

  • Latent infection in nerve cells; periodic reactivation causes outbreaks.

• Diagnosis: Presence of characteristic lesions.

• Prevention: Gloves for healthcare workers; avoid contact with lesions.

• Epidemiology:

  • HHV-1: usually acquired in childhood; 80% of children worldwide by age 2.

  • HHV-2: acquired between ages 15-29, often sexually transmitted.

  • Both can be spread between oral and genital mucous membranes.

  • Herpes whitlow: risk for thumb-suckers, dental professionals.

  • Neonatal infections can be fatal.