Viruses, Viroids, and Prions: Structure, Classification, and Pathogenicity

Viruses, Viroids, and Prions

Distinctive Features of Viruses

Viruses are unique infectious agents that differ fundamentally from cellular organisms. They are obligatory intracellular parasites, meaning they require living host cells to multiply. Viruses contain either DNA or RNA as their genetic material, but never both. Their structure includes a protein coat (capsid), and they lack ribosomes and an ATP-generating mechanism, relying entirely on the host cell's machinery for replication.

• Obligatory intracellular parasites: Must invade host cells to reproduce.

• Genetic material: DNA or RNA, single- or double-stranded, linear, circular, or segmented.

• Protein coat: Protects genetic material and aids in host cell attachment.

• No ribosomes or ATP-generating mechanism: Cannot synthesize proteins or generate energy independently.

Host Range

The host range of a virus refers to the spectrum of host cells it can infect. Most viruses are highly specific, infecting only certain cell types within a host. This specificity is determined by the presence of particular attachment sites on the host cell and compatible cellular factors.

• Bacteriophages: Infect bacteria; receptor sites may be on cell wall, fimbriae, or flagella.

• Animal viruses: Receptor sites are typically on the plasma membrane.

Virus Sizes

Viruses vary greatly in size, typically ranging from 20 nm to 300 nm. Their small size allows them to pass through bacteriological filters that retain bacteria.

Viral Structure

The virion is the complete, fully developed viral particle. Its structure includes:

• Nucleic acid: DNA or RNA, single- or double-stranded, linear, circular, or segmented.

• Capsid: Protein coat made of capsomeres (subunits).

• Envelope: Lipid, protein, and carbohydrate coating present in some viruses.

• Spikes: Projections from the outer surface, often used for attachment.

Capsid and Envelope

The capsid is composed of protein subunits called capsomeres. Some viruses possess an envelope external to the capsid, derived partly from the host cell's plasma membrane during viral budding. Spikes on the envelope may facilitate attachment to host cells.

General Morphology of Viruses

Viruses are classified by their morphology:

• Helical viruses: Hollow, cylindrical capsid; e.g., rabies and Ebola viruses.

• Polyhedral viruses: Many-sided, most commonly icosahedral; e.g., adenoviruses, poliovirus.

• Enveloped viruses: Usually spherical.

• Complex viruses: Complicated structures; e.g., bacteriophages.

Taxonomy and Classification of Viruses

Viruses are classified based on their genetic material and replication strategy. The Baltimore classification system divides viruses into seven groups (realms) according to their nucleic acid type and how mRNA is produced. Viral taxonomy uses the following conventions:

• Genus: Ends in -virus

• Family: Ends in -viridae

• Order: Ends in -ales

• Viral species: Group sharing genetic information and ecological niche

Growing Viruses in the Laboratory

Bacteriophages

Bacteriophages are grown in bacteria, forming plaques (clearings) on a lawn of bacteria on agar. Each plaque corresponds to a single virus and is quantified as plaque-forming units (PFU).

Animal Viruses

• In living animals: Mice, rabbits, guinea pigs; some human viruses may not cause disease in animals.

• In embryonated eggs: Virus injected into egg; growth signaled by changes or embryo death; used for vaccine production.

• In cell cultures: Primary cell lines (from tissues), diploid cell lines (from embryos), and continuous cell lines (from cancerous cells, e.g., HeLa).

• Cytopathic effect (CPE): Visible changes or deterioration in monolayer cells due to viral infection.

Viral Identification

Viruses are identified by:

• Cytopathic effects: Observed in cell culture.

• Serological tests: ELISA detects viruses by antibody reactions.

• Nucleic acid tests: PCR amplifies viral genetic material for identification.

Viral Multiplication

To multiply, a virus must invade a host cell and commandeer its metabolic machinery. A single virion can produce thousands of progeny in one cell. The one-step growth curve illustrates the stages of viral replication.

Comparison of Bacteriophage and Animal Viral Multiplication

Stage	Bacteriophages	Animal Viruses
Attachment	Tail fibers attach to cell wall proteins	Receptor sites are plasma membrane proteins and glycoproteins
Entry	Viral DNA is injected into host cell	Capsid enters by receptor-mediated endocytosis or fusion
Uncoating	Not required	Enzymatic removal of capsid proteins
Biosynthesis	In cytoplasm	In nucleus (DNA viruses) or cytoplasm (RNA viruses)
Chronic infection	Lysogeny	Latency; slow viral infections; cancer
Release	Host cell is lysed	Enveloped viruses bud out; nonenveloped viruses rupture plasma membrane

Multiplication of Animal Viruses

The process includes:

• Attachment: Virus binds to cell membrane.

• Entry: Via receptor-mediated endocytosis or fusion.

• Uncoating: Viral nucleic acid separated from capsid by enzymes.

• Biosynthesis: Production of viral nucleic acid and proteins.

• Maturation: Assembly of nucleic acid and capsid proteins.

• Release: By budding (enveloped viruses) or rupture (nonenveloped viruses).

Viruses and Cancer

Some viruses are oncogenic, meaning they can cause cancer. Viral-induced cancers may develop long after infection and are not contagious. Types include:

• Sarcoma: Cancer of connective tissue.

• Adenocarcinomas: Cancer of glandular epithelial tissue.

Transformation of Normal Cells Into Tumor Cells

• Proto-oncogenes: Genes encoding proteins for normal cell growth; mutations convert them to oncogenes.

• Oncogenic viruses: Integrate into host DNA, inducing tumors.

• Transformed cells: Exhibit tumor-specific antigens and irregular shapes.

DNA Oncogenic Viruses

• Adenoviridae

• Herpesviridae: Epstein-Barr virus (Burkitt’s lymphoma)

• Poxviridae

• Papovaviridae: Human papillomavirus (HPV; cervical and anal cancer)

• Hepadnaviridae: Hepatitis B virus

RNA Oncogenic Viruses

• Retroviridae: Viral RNA transcribed to DNA (reverse transcriptase), integrates into host DNA. HTLV-1 and HTLV-2 cause adult T cell leukemia and lymphoma; FeLV causes feline leukemia.

Latent and Persistent Viral Infections

Viruses may establish latent or persistent infections:

• Latent infections: Virus remains dormant in host cell; may reactivate (e.g., herpesviruses, cold sores, shingles).

• Persistent infections: Virus is continuously released; often fatal (e.g., HIV/AIDS, hepatitis B, measles).

Disease	Primary Effect	Causative Virus
Cold sores	Skin and mucous membrane lesions; genital lesions	HHV-1 and HHV-2
Leukemia	Increased white blood cell growth	HTLV-1 and -2
Shingles	Skin lesions	Varicellovirus (Herpesvirus)
Cervical cancer	Increased cell growth	Human papillomavirus
HIV/AIDS	Decreased CD4+ T cells	HIV-1 and -2 (Lentivirus)
Liver cancer	Increased cell growth	Hepatitis B virus
Persistent enterovirus infection	Mental deterioration associated with AIDS	Echoviruses
Progressive encephalitis	Rapid mental deterioration	Rubella virus
Subacute sclerosing panencephalitis (SSPE)	Mental deterioration	Measles virus

Prions

Prions are infectious proteins, inherited and transmissible by ingestion, transplant, or surgical instruments. They cause spongiform encephalopathies such as "mad cow disease," Creutzfeldt-Jakob disease (CJD), and sheep scrapie. Disease results from the conversion of normal cellular prion protein (PrPC) into an infectious misfolded form (PrPSc), which accumulates in brain cells, forming plaques.

Viruses vs. Bacteria

Property	Bacteria	Viruses
Intracellular Parasite	No (typical), Yes (Rickettsias/Chlamydias)	Yes
Plasma Membrane	Yes	No
Binary Fission	Yes	No
Pass through Bacteriological Filters	No/Yes	Yes
Possess Both DNA and RNA	Yes	No
ATP-Generating Metabolism	Yes/No	No
Ribosomes	Yes	No
Sensitive to Antibiotics	Yes	No
Sensitive to Interferon	No	Yes

Summary

This chapter provides a comprehensive overview of viruses, viroids, and prions, including their structure, classification, replication, laboratory cultivation, pathogenicity, and comparison with bacteria. Understanding these agents is essential for microbiology students, as they play significant roles in infectious diseases, cancer, and neurodegenerative disorders.