A-type inclusion bodies: a factor influencing cowpox virus lesion pathogenesis

Juliana Almeida Leite1, Flávio Guimarães da Fonseca, Giliane de Souza Trindade

  • 1Laboratório de Vírus, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos 6627, Belo Horizonte, MG, Brazil. juufmg@yahoo.com.br

Archives of Virology
|January 8, 2011
PubMed

Insights

A-type inclusion bodies (ATIs) are not essential for cowpox virus replication in vitro. However, their absence impacts lesion progression in vivo, suggesting a role in healing dynamics.

Area of Science:

  • Virology
  • Molecular Biology
  • Animal DNA Viruses

Background:

  • Poxviridae are complex animal DNA viruses.
  • A-type inclusion bodies (ATIs) are produced during some poxvirus infections.
  • The biological function of ATIs remains poorly understood.

Purpose of the Study:

  • To investigate the biological role of ATIs in cowpox virus replication.
  • To compare the in vitro and in vivo behavior of wild-type and ATI-deleted cowpox viruses.

Main Methods:

  • Construction of a recombinant ati-deleted cowpox virus.
  • In vitro assays: electron microscopy, plaque assays, viral growth assays.
  • In vivo analysis: macroscopic and histological examination of lesion progression.

Main Results:

  • No significant differences in viral replication or morphogenesis were observed in vitro.
  • The inclusion body is not essential for in vitro viral replication.
  • Distinct lesion progression dynamics were observed in vivo between wild-type and ATI-deleted viruses.

Conclusions:

  • ATIs are not essential for cowpox virus in vitro replication.
  • The presence or absence of ATIs influences healing dynamics during in vivo infection.
  • This study uniquely isolates the role of ATIs by comparing viruses solely based on their presence or absence.

Related Concept Videos

Smallpox01:24

Smallpox

Smallpox is a severe contagious disease caused by the Variola major virus, a double-stranded DNA member of the Poxviridae family.Variola major transmission occurs primarily via inhalation of virus-laden droplets or direct contact with infectious scabs. The incubation period averages approximately seven days, although it may range from 7 to 17 days depending on the inoculum and host factors.Clinically, the prodromal phase is marked by an abrupt onset of high fever, malaise, headache, and myalgia.
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Subviral Agents01:29

Subviral Agents

Subviral agents are infectious entities that resemble viruses but lack one or more viral components, such as a capsid or essential replication machinery. These agents include viroids, prions, and satellites, each possessing distinct structural and functional characteristics that influence their mode of infection and replication.Viroids are the simplest subviral agents, consisting of circular, single-stranded RNA molecules without a protein coat. They exclusively infect plants, relying entirely...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...