Virology

🦠Virology Unit 8 – Human Viral Pathogens – DNA Viruses

DNA viruses are a diverse group of pathogens that cause various human diseases. These viruses contain DNA genomes, replicate in the host cell nucleus, and employ complex strategies to evade immune responses and persist in the body. Understanding DNA viruses is crucial for developing effective treatments and prevention methods. From common cold sores to cancer-causing infections, these viruses significantly impact human health and require ongoing research to combat their effects.

Introduction to DNA Viruses

  • DNA viruses contain a genome composed of double-stranded DNA (dsDNA) or single-stranded DNA (ssDNA)
  • Possess a protein capsid that encases and protects the viral genome
  • May have an additional lipid envelope derived from the host cell membrane
  • Replicate within the nucleus of the host cell, utilizing host cell machinery for transcription and replication
  • Cause a wide range of diseases in humans, including respiratory illnesses, skin infections, and various cancers
  • Examples of DNA viruses include Herpesviruses (Epstein-Barr virus), Adenoviruses, and Papillomaviruses (Human Papillomavirus)

Viral Structure and Genome

  • DNA viruses have a genome made of DNA, which can be linear or circular, and single-stranded or double-stranded
    • Linear genomes have free ends, while circular genomes form a continuous loop
    • Double-stranded DNA is more stable and less prone to mutations compared to single-stranded DNA
  • Genome size varies among DNA viruses, ranging from a few kilobases (kb) to hundreds of kilobases
  • Viral capsid is composed of multiple copies of one or more types of capsid proteins, which self-assemble to form a protective shell around the genome
    • Capsid proteins are encoded by the viral genome and synthesized during replication
  • Some DNA viruses (Herpesviruses) have an additional lipid envelope surrounding the capsid, which is derived from the host cell membrane during the budding process
  • Structural proteins, such as tegument proteins in Herpesviruses, may be present between the capsid and the envelope, providing additional functions in the viral life cycle

Replication Cycle

  • Attachment: Viral surface proteins (capsid or envelope proteins) bind to specific receptors on the host cell surface
  • Entry: Viruses enter the cell through endocytosis or fusion with the cell membrane, releasing the capsid into the cytoplasm
  • Uncoating: The viral capsid is disassembled, exposing the viral genome
  • Replication: The viral genome is transported to the nucleus, where it is transcribed and replicated using host cell machinery
    • Early genes are expressed first, encoding proteins required for viral genome replication and regulation of host cell functions
    • Late genes are expressed after genome replication, encoding structural proteins for new virion assembly
  • Assembly: Newly synthesized viral proteins and genomes are assembled into progeny virions within the nucleus
  • Maturation: Virions undergo further modifications, such as the acquisition of tegument proteins and envelopes (in Herpesviruses)
  • Release: Mature virions are released from the host cell through lysis or budding, ready to infect new cells

Major DNA Virus Families

  • Herpesviridae: Large, enveloped dsDNA viruses that establish latent infections (Herpes Simplex Virus, Varicella-Zoster Virus, Cytomegalovirus)
  • Adenoviridae: Non-enveloped dsDNA viruses that cause respiratory, gastrointestinal, and eye infections (Adenovirus)
  • Papillomaviridae: Small, non-enveloped dsDNA viruses that infect epithelial cells and are associated with various cancers (Human Papillomavirus)
  • Polyomaviridae: Small, non-enveloped dsDNA viruses that can cause tumors and multisystem diseases (JC virus, BK virus)
  • Poxviridae: Large, complex dsDNA viruses that replicate in the cytoplasm (Smallpox virus, Molluscum Contagiosum virus)
  • Parvoviridae: Small, non-enveloped ssDNA viruses that depend on helper viruses or cellular factors for replication (Parvovirus B19)

Pathogenesis and Disease

  • DNA viruses employ various strategies to enter, replicate, and spread within the host, leading to disease
  • Viral entry and replication can directly damage host cells through lysis or apoptosis
  • Viral proteins can interfere with host cell functions, such as cell cycle regulation, leading to uncontrolled cell growth and cancer (Papillomaviruses, Polyomaviruses)
  • Immune-mediated pathology: Host immune response to viral infection can cause inflammation and tissue damage
    • Cytokine storm: Overproduction of pro-inflammatory cytokines can lead to systemic inflammation and organ dysfunction
  • Latency: Some DNA viruses (Herpesviruses) can establish latent infections, persisting in the host for long periods without causing symptoms
    • Reactivation of latent viruses can lead to recurrent disease (cold sores, shingles)
  • Oncogenesis: Certain DNA viruses (Papillomaviruses, Epstein-Barr virus) can transform infected cells, leading to the development of cancers

Immune Response and Evasion

  • Innate immune response: Early, non-specific defense against viral infection
    • Type I interferons (IFN-α/β) are produced by infected cells, inducing an antiviral state in neighboring cells
    • Natural killer (NK) cells recognize and kill virus-infected cells
  • Adaptive immune response: Specific, long-lasting immunity mediated by T and B lymphocytes
    • CD8+ cytotoxic T cells recognize and eliminate virus-infected cells
    • CD4+ helper T cells support cytotoxic T cell and B cell responses
    • B cells produce virus-specific antibodies that neutralize viruses and mark infected cells for destruction
  • DNA viruses have evolved various mechanisms to evade host immune responses
    • Inhibition of antigen presentation: Viral proteins can interfere with MHC class I expression, preventing recognition by cytotoxic T cells (Herpesviruses)
    • Mimicry of host immune regulators: Viruses can produce proteins that resemble host immunomodulatory molecules, suppressing immune responses (Poxviruses)
    • Interference with apoptosis: Viral proteins can block apoptosis of infected cells, allowing continued viral replication (Adenoviruses)

Diagnosis and Detection

  • Clinical presentation: Diagnosis based on characteristic signs and symptoms of viral infection
  • Serological tests: Detection of virus-specific antibodies (IgM, IgG) in patient serum
    • Enzyme-linked immunosorbent assay (ELISA): Quantitative measurement of antibody levels
    • Immunofluorescence assay (IFA): Visualization of antibody binding to virus-infected cells
  • Viral antigen detection: Identification of viral proteins in clinical samples using antibodies
    • Direct fluorescent antibody (DFA) test: Fluorescently labeled antibodies bind to viral antigens in infected cells
  • Molecular methods: Detection of viral nucleic acids in clinical samples
    • Polymerase chain reaction (PCR): Amplification and detection of viral DNA sequences
    • Real-time PCR: Quantitative measurement of viral load
  • Viral culture: Isolation and growth of the virus in cell culture systems, followed by identification using immunological or molecular methods

Treatment and Prevention

  • Antiviral drugs: Medications that inhibit viral replication or block viral entry into host cells
    • Acyclovir and valacyclovir: Nucleoside analogs that inhibit Herpesvirus DNA polymerase
    • Cidofovir: Nucleotide analog that inhibits viral DNA polymerase in Adenoviruses and Poxviruses
  • Immunoglobulins: Passive immunization using preformed antibodies to neutralize viruses or modulate immune responses
  • Vaccines: Active immunization to prevent viral infections
    • Live attenuated vaccines: Weakened viral strains that induce immunity without causing disease (Varicella vaccine)
    • Inactivated vaccines: Killed viruses that stimulate an immune response (Hepatitis A vaccine)
    • Subunit vaccines: Purified viral proteins that elicit protective immunity (Hepatitis B vaccine)
    • Virus-like particle (VLP) vaccines: Self-assembling viral capsid proteins that mimic the structure of the virus (Human Papillomavirus vaccine)
  • Infection control measures: Practices to prevent the spread of viral infections
    • Hand hygiene, personal protective equipment (gloves, masks), and proper disinfection of surfaces
    • Isolation of infected individuals to minimize transmission


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© 2024 Fiveable Inc. All rights reserved.
AP® and SAT® are trademarks registered by the College Board, which is not affiliated with, and does not endorse this website.