Video Experimental Relacionado
Updated: Aug 18, 2026
13:22
Measurement of γHV68 Infection in Mice
Published on: November 22, 2011
Conversión de la infección por alfavirus lítico a persistente por el oncogén celular bcl-2
B Levine1, Q Huang, J T Isaacs
1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-7681.
Nature
|February 25, 1993
Resumen
La infección por el virus Sindbis (SV) desencadena la muerte celular programada en las células no neuronales. Sin embargo, la expresión del oncogén bcl-2 previene esto, estableciendo infecciones virales persistentes al bloquear la apoptosis.
Área de la Ciencia:
- Virología Virología.
- Biología celular Biología celular.
- Oncología Oncología.
Sus antecedentes:
- Las interacciones entre virus y huésped que rigen el potencial lítico viral siguen siendo poco conocidas.
- El virus Sindbis (SV) típicamente causa infecciones líticas pero establece infecciones persistentes en las neuronas.
- El oncogén bcl-2 inhibe la apoptosis, un factor clave en la muerte celular.
Objetivo del estudio:
- Para investigar si la infección por SV induce apoptosis en las células no neuronales.
- Para determinar si bcl-2 puede bloquear la apoptosis inducida por SV.
- Explorar el papel de bcl-2 en el establecimiento de infecciones virales persistentes.
Principales métodos:
- Infección de las células del riñón del hámster bebé (BHK-2), el neuroblastoma de ratón (N18) y el adenocarcinoma prostático de rata (AT-3) con SV.
- Transfección de las células AT-3 con el oncogén bcl-2.
- Monitoreo de la muerte celular y la replicación viral después de la infección.
Principales resultados:
- La infección por SV indujo la muerte celular programada (apoptosis) en las células BHK-2, N18 y AT-3.
- La infección por SV de las células AT-3 transfectadas con bcl-2-resultó en una infección productiva persistente a largo plazo.
- El bloqueo de la apoptosis a través de la expresión de bcl-2 evitó la muerte celular inducida por SV.
Conclusiones:
- La infección por SV desencadena la apoptosis en las células no neuronales susceptibles.
- La expresión celular del oncogén bcl-2 es crucial para establecer una infección persistente por SV.
- El bloqueo de la apoptosis inducida por el virus es un mecanismo clave para la persistencia viral.
Más Videos Relacionados
10:01Radial Mobility and Cytotoxic Function of Retroviral Replicating Vector Transduced, Non-adherent Alloresponsive T Lymphocytes
Published on: February 11, 2015
07:10Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
Published on: August 15, 2025
Videos de Conceptos Relacionados
01:30Lytic Cycle of Bacteriophages
Bacteriophages, also known as phages, are specialized viruses that infect bacteria. A key characteristic of phages is their distinctive “head-tail” morphology. A phage begins the infection process (i.e., lytic cycle) by attaching to the outside of a bacterial cell. Attachment is accomplished via proteins in the phage tail that bind to specific receptor proteins on the outer surface of the bacterium. The tail injects the phage’s DNA genome into the bacterial cytoplasm. In the lytic replication...
00:43Lysogenic Cycle of Bacteriophages
In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
01:10Retrovirus Life Cycles
Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
01:51Mechanisms of Retrovirus-induced Cancers
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
01:03Rous Sarcoma Virus (RSV) and Cancer
Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
01:28Rabies
Rabies is a lethal zoonotic disease caused by a single-stranded, negative-sense RNA virus of the Lyssavirus genus, within the family Rhabdoviridae. Its primary mode of transmission to humans is through bites or saliva-contaminated scratches from infected mammals such as dogs, bats, raccoons, or foxes. Transmission can also occur if infectious saliva contacts abraded skin or intact mucous membranes, including the conjunctiva.Viral Entry and Early ReplicationOnce introduced at the bite or scratch...