Picornavirus Tropism
Picornavirus Tropism - Related Videos
09:05
MicroRNA-based Regulation of Picornavirus Tropism
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Cited by 4 •
2017
We describe here a method for regulating picornavirus tropism by incorporating sequences complementary to specific microRNAs into the viral genome. This protocol can be adapted to all different classes of viruses with modifications based upon the length and nature of their life cycle.
11:10
Genotypic Inference of HIV-1 Tropism Using Population-based Sequencing of V3
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Cited by 20 •
2010
HIV tropism can be inferred from the V3 region of the viral envelope. V3 is PCR amplified in triplicate using nested RT-PCR, sequenced, and interpreted using bioinformatic software. Samples with with 1 or more sequence(s) with low g2P scores are classified as non-R5 virus.
07:06
Prediction of HIV-1 Coreceptor Usage (Tropism) by Sequence Analysis using a Genotypic Approach
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Cited by 16 •
2011
The prediction of the coreceptor usage of HIV-1 is required for the administration of a new class of antiretroviral drugs, i.e. coreceptor antagonists. It can be performed by sequence analysis of the env gene and subsequent interpretation through an internet based interpretation system (geno2pheno[coreceptor]).
03:52
Suspension Culture Production and Purification of Adeno-Associated Virus by Iodixanol Density Gradient Centrifugation for In Vivo Applications
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Cited by 3 •
2024
Adeno-associated virus is produced in suspension cell culture and purified by double iodixanol density gradient centrifugation. Steps are included to increase total virus yield, decrease the risk of virus precipitation, and further concentrate the final virus product. Expected final titers reach 1012 viral particles/mL and are suitable for pre-clinical in vivo use.
05:31
Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
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Cited by 4 •
2017
This protocol describes a noninvasive technique for the sampling of undisturbed mucosal lining fluid from the upper airways. It can be used to perform the quantification of in vivo levels of protein mediators, such as cytokines and chemokines, in subjects of all ages.
FAQs
Capsid proteins help determine whether a picornavirus can interact with receptors on a host cell. This interaction influences which cells are accessible to the virus and therefore where infection can begin. Receptor differences among tissues, organs, or host species can produce distinct infection patterns, making capsid-receptor compatibility an important determinant of host range and disease distribution.
Receptor binding alone does not establish productive infection. After entry, the virus depends on intracellular factors that support genome translation, genome replication, and release of newly produced virus. Cells that permit these processes can sustain infection, whereas cells lacking suitable intracellular support may restrict the infection even when viral attachment or entry is possible.
Tissue-specific antiviral responses can limit infection after a virus reaches a potentially susceptible cell. Their strength or character may influence whether infection remains restricted or develops within a particular tissue. Consequently, tropism reflects more than receptor availability and viral replication capacity; local antiviral activity also helps determine the extent and outcome of infection.
Related picornaviruses may differ in the tissues and organs they successfully infect because their capsid-receptor interactions, intracellular requirements, and sensitivity to tissue-specific antiviral responses are not identical. These differences can shift disease involvement toward respiratory, gastrointestinal, neurologic, hepatic, or mucocutaneous sites, helping explain varied clinical patterns among related viruses.
A tropism study can examine several linked determinants: capsid interactions with cell-surface receptors, intracellular support for genome translation and replication, viral release, and tissue-specific antiviral responses. Considering these factors together helps researchers assess why infection develops in particular cells or organs and provides a framework for evaluating host-range patterns and disease-associated tissue involvement.
Tropism information helps connect viral characteristics with the tissues involved during disease, making it useful for pathogenesis studies. It also informs animal-model selection by indicating whether a prospective host and its tissues can reflect relevant infection patterns. This context supports more focused investigation of disease development and host-range assessment across picornaviruses.
Understanding the determinants of tropism identifies biological features linked to tissue infection and viral spread. That knowledge supports vaccine and antiviral development by clarifying relevant infection processes, while also informing the design of engineered viral vectors. In each case, tropism provides a way to relate viral targeting and replication behavior to the intended research or therapeutic application.