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Viruses Notes

Viruses are non-cellular infectious agents characterized by a nucleic acid core (DNA or RNA) surrounded by a protective protein coat called a capsid. This nucleocapsid can sometimes be further enclosed by a viral envelope, derived from host cell membranes and studded with viral glycoproteins. Viruses are obligate intracellular parasites, meaning they are metabolically inert outside a host cell and absolutely require host cellular machinery for their replication and survival. They range significantly in size, typically from 20\,nm to 400\,nm. Viral life cycles encompass both lytic and lysogenic (or latent) phases, dictating their interaction with host cells.

Viral Shapes and Hosts

Viral shapes are diverse, primarily classifying into:

  • Helical: Rod-shaped or filamentous, with capsomeres arranged helically around the nucleic acid (e.g., Tobacco Mosaic Virus, Rabies Virus).

  • Icosahedral: Polyhedral, nearly spherical, with 20 triangular faces (e.g., Adenovirus, Herpes Simplex Virus).

  • Complex: Possessing structures that are neither purely helical nor icosahedral (e.g., Bacteriophages with head-and-tail structures, Poxviruses).
    Each virus has a specific host range, referring to the types of organisms or cells it can infect. They also exhibit tissue tropism, meaning they infect specific cell types within a host due to the specific interaction between viral surface proteins (e.g., spikes, fusion proteins) and complementary host cell receptors. For instance, the rabies virus specifically targets neurons, while influenza virus primarily targets respiratory epithelial cells.

Viral Genomes

Viral genomes display remarkable diversity and can be composed of either DNA or RNA, which can be single-stranded (SS) or double-stranded (DS). Importantly, RNA viruses generally replicate in the cytoplasm, often utilizing their own RNA-dependent RNA polymerase, leading to higher mutation rates due to the lack of proofreading. Examples include influenza (+/- ssRNA) and poliovirus (+ssRNA). DNA viruses, like Herpes Simplex Virus (dsDNA), typically replicate in the nucleus, hijacking host DNA replication machinery. Viral genomes can also be linear, circular, or segmented. Some RNA viruses, known as retroviruses (e.g., HIV), carry an enzyme called reverse transcriptase to convert their RNA genome into DNA, which then integrates into the host cell's genome as a provirus.

Viral Replication

Viruses inherently lack the cellular machinery (e.g., ribosomes, ATP-generating system) for self-replication and must entirely hijack host cellular processes. The comprehensive viral life cycle typically includes several stages, often resulting in damage to host cells (cytopathic effects):

  1. Attachment (Adsorption): Specific binding of viral surface proteins to complementary receptor molecules on the host cell surface.

  2. Penetration (Entry): The virus enters the host cell through various mechanisms such as direct fusion of the viral envelope with the plasma membrane, receptor-mediated endocytosis, or direct injection of the nucleic acid (common in bacteriophages).

  3. Uncoating: The viral capsid is removed, releasing the viral nucleic acid into the host cell cytoplasm or nucleus.

  4. Synthesis (Replication): Viral genome replication and transcription, followed by translation of viral proteins, utilizing the host's ribosomes and metabolic machinery. This often involves early gene expression for replication enzymes and late gene expression for structural proteins.

  5. Assembly (Maturation): New viral nucleic acids and proteins are assembled into progeny virions.

  6. Release: New viruses exit the host cell, either by budding (for enveloped viruses, often without immediate cell lysis) or by lysis (rupture) of the host cell (for non-enveloped viruses and bacteriophages), releasing many virions.

Viral Infections and Diseases

Viral infections manifest in various ways and can be broadly categorized as acute or persistent:

  • Acute Infections: Characterized by rapid viral replication, rapid onset of symptoms, and typically a rapid resolution (e.g., influenza, common cold caused by rhinovirus, SARS-CoV-2).

  • Persistent Infections: The virus remains in the host for long periods, sometimes for life. These can be:

    • Latent: The virus remains dormant for periods, integrating its genome or existing as an episome, with periodic reactivation (e.g., Herpes Simplex Viruses causing cold sores, Varicella-Zoster Virus causing chickenpox and shingles).

    • Chronic: Continuous shedding of the virus, detectable for long periods, sometimes without severe symptoms (e.g., Hepatitis B and C viruses).

    • Slow: Long incubation period, followed by a slow progressive disease (e.g., HIV/AIDS).
      Many pathogenic viruses cause diseases ranging from mild to severe, impacting plants, animals, and humans. Some viruses are also significant oncogenic viruses, directly linked to various cancers, such as Human Papillomavirus (HPV) causing cervical and other anogenital cancers, Epstein-Barr Virus (EBV) linked to Burkitt's lymphoma and nasopharyngeal carcinoma, and Hepatitis B and C viruses (HBV, HCV) associating with hepatocellular carcinoma.

Phage Dynamics

Bacteriophages (phages) are viruses that infect bacteria. They can undertake two primary life cycles:

  • Lytic Cycle: The phage immediately hijacks the host bacterial cell's machinery to produce new phage particles, leading to rapid bacterial cell lysis and release of progeny phages.

  • Lysogenic Cycle: The viral DNA (prophage) integrates with the host bacterial genome or remains as a stable plasmid. It replicates along with the host chromosome without immediately killing the cell. The prophage can be excised from the host genome and initiate a lytic cycle under certain environmental stresses (e.g., UV radiation). This process can also lead to lysogenic conversion, where the prophage confers new properties to the host bacterium, such as toxin production.

Viroids and Prions

Beyond conventional viruses, other infectious agents exist:

  • Viroids: Small, circular, single-stranded RNA molecules that are infectious and cause various diseases, primarily in plants (e.g., potato spindle tuber viroid). They lack a protein coat and rely entirely on host cell enzymes (often host RNA polymerase) for their replication.

  • Prions: Infectious, misfolded proteins (proteinaceous infectious particles) that are devoid of nucleic acids. They are responsible for a group of fatal neurodegenerative diseases called Transmissible Spongiform Encephalopathies (TSEs), such as Creutzfeldt-Jakob Disease (CJD) in humans, Bovine Spongiform Encephalopathy (BSE) in cattle, and scrapie in sheep. Prions propagate by inducing normal cellular prion proteins (PrP^C) to misfold into the infectious, aggregation-prone form (PrP^{Sc}), leading to amyloid plaques and neuronal damage. They are highly resistant to inactivation by conventional sterilization methods.

Epidemiology and Classification

Viruses are classified through several systems. The International Committee on Taxonomy of Viruses (ICTV) provides a universal classification system based on characteristics such as morphology, genetic material, replication strategies, and host range. Another crucial classification system is the Baltimore Classification, which categorizes viruses into seven groups based on their type of genome (DNA/RNA, SS/DS) and their method of mRNA synthesis, providing insights into their replication mechanisms. Viral epidemiology studies the patterns, causes, and effects of viral diseases in populations, considering transmission routes (e.g., direct contact, aerosol, vector-borne), reservoirs, and factors influencing epidemics and pandemics.