LW

Unit 2 Lecture 2

Viral Activity and Host Range

  • Active State: When a virus becomes active, it starts making viral proteins, forcing the host cells to produce viral components, leading to the creation of new viral particles.

  • Host Range: Refers to the types of cells or species a virus can infect.

    • Moderately Restricted Host Range: An example is Poliovirus, which can infect the intestines and nerve cells of any primate (humans, apes, chimps, monkeys), indicating a broader scope than just a single species.

    • Wide Host Range: Rabies virus can infect any mammal (skunks, bats, dogs, etc.), highlighting a very broad range of potential hosts.

Viral Entry and Host Defense Mechanisms

  • Entry: Viruses typically enter by attaching to the cell membrane, after which the capsid is broken down, releasing their genetic material (DNA or RNA) into the cell.

  • Difficulty in Stopping Viral Infection: Once the viral genetic material is inside the cell, it becomes much more difficult to stop the infection.

  • Host Defense Systems within Cells: Our cells are not defenseless; they possess mechanisms to fight off invading viruses.

    • Single Virus Scenario: If just one virus enters a cell, it will likely be destroyed by intracellular mechanisms such as lytic enzymes and lysosomes.

    • Typical Infection Scenario: Usually, hundreds of viruses land on a cell, and more than just one may sneak in.

    • Success Threshold: Only a single viral genetic material (DNA or RNA) is needed to successfully infect the nucleus of a eukaryotic cell or the nucleoid of a bacterial or archaeal cell and initiate replication.

Viral Replication and Protein Synthesis

  • Hijacking Host Machinery: Viruses commandeer the host cell's machinery for protein synthesis.

    • DNA Viruses: The viral DNA enters the nucleus, where it is read by host enzymes just like host DNA, leading to the production of viral messenger RNA (mRNA).

    • RNA Viruses: Viral RNA can directly act as mRNA or be used as a template to synthesize mRNA. This viral mRNA then travels to the ribosomes.

    • Protein Production: At the ribosomes, the viral mRNA is read, leading to the synthesis of viral proteins instead of host proteins.

Viral Assembly and Release

  • Adsorption: The virus first attaches to the host cell.

  • Penetration and Uncoating: The virus enters the cell, and its outer coating (capsid) is removed, releasing the viral genetic material (e.g., RNA).

  • Synthesis: The viral genetic material integrates with or utilizes the host's genetic machinery (e.g., incorporating into the host mRNA transcription process), tricking the cell into synthesizing new viral components such as spikes, capsomeres (for the capsid), and new nucleic acids.

  • Assembly: These newly synthesized viral components are then reassembled into complete viral particles within the host cell's cytoplasm.

  • Release Mechanisms:

    • Enveloped Viruses (e.g., Herpesviruses): After assembly, these viruses acquire a new envelope by budding off from the host cell membrane, taking a portion of the host's phospholipids. This process allows many new viral particles to be released from a single infected cell without immediately killing it.

    • Non-Enveloped Viruses (e.g., Bacteriophages): These viruses replicate until the host cell becomes overloaded. The cell's membrane or wall is then weakened, causing it to rupture (lysis), which releases thousands of new viral particles and kills the cell.

Diagnosing Viral Infections: Cytopathic Effects (CPEs)

  • Microscopic Limitations: Viruses themselves are generally too small to be seen with standard light microscopy.

  • Identifying Infection: Viral infections are often diagnosed by observing visible changes in the host cells, known as cytopathic effects (CPEs).

  • Common CPEs:

    • Changes in Shape and Size: Infected cells may appear abnormally shaped, larger, or smaller than healthy cells.

    • Inclusion Bodies: These are characteristic masses of viral particles or damaged cellular organelles that accumulate inside the infected cells.

    • Syncytia: A significant indicator of viral infection is the fusion of multiple infected cells into a large, multinucleated giant cell. This phenomenon is abnormal (cells should typically be individual or in connected tissues, not clumped) and suggests viral presence.

  • Specific Example: Cytomegalovirus can cause syncytia and inclusion bodies in the cytoplasm.

Latency and Reactivation (Provirus/Lysogenic State)

  • Provirus/Lysogenic State: Some viruses, known as proviruses, integrate their genetic material (DNA or RNA) into the host cell's DNA and remain dormant or inactive for extended periods.

    • During dormancy, the virus does not immediately lyse the cell or produce new viral particles; it simply replicates along with the host cell's DNA during cell division.

  • Reactivation: The latent virus can be triggered to become active again by various factors, including stress, certain foods, or other unknown stimuli. These triggers can cause the virus to transition into a lytic cycle, producing new viral particles and symptoms.

  • Examples of Latent Viruses:

    • Herpes Simplex Virus (Cold Sores): Lives dormantly in nerve cells. Reactivation causes cold sores to erupt at the same spot. It then returns to dormancy.

    • Varicella-Zoster Virus (Chickenpox/Shingles): Causes chickenpox in childhood and can reactivate later in life as shingles.

    • Hepatitis C: Can enter a state of remission and then reactivate, causing inflammation and symptoms.

Oncoviruses: Viruses that Cause Cancer

  • Definition: