In what respect does the genome of slow-acting retroviruses differ from those of transducing viruses?
They lack an oncogene
Retroviruses are a family of RNA viruses that replicate by using a reverse transcriptase enzyme to produce DNA from their RNA genome. This DNA is then integrated into the host cell's genome.
Retroviruses can be classified based on how they cause disease, particularly cancer. Two important types are slow-acting retroviruses and transducing retroviruses.
Transducing retroviruses are known for their ability to cause tumors rapidly. This is because their genome typically includes a viral oncogene (v-onc). This oncogene is often acquired from a cellular proto-oncogene (c-onc) through a process involving recombination during replication. Once integrated into the host cell, the viral oncogene is expressed, leading to uncontrolled cell growth and tumor formation.
Slow-acting retroviruses, unlike transducing retroviruses, generally do not carry their own oncogene in their genome. Their mechanism for causing cancer is different and takes longer (hence "slow-acting"). They integrate their proviral DNA into the host cell's genome. If the integration site is near a cellular proto-oncogene, the strong viral regulatory elements (like promoters and enhancers, typically found in the viral LTRs or Long Terminal Repeats) can cause overexpression or abnormal expression of the cellular proto-oncogene. This deregulation of the proto-oncogene can then lead to cell transformation and cancer.
The fundamental difference in the genome between slow-acting retroviruses and transducing retroviruses lies in the presence or absence of an oncogene.
While slow-acting retroviruses can cause cancer by affecting nearby cellular proto-oncogenes after integration, their inherent genome structure is characterized by the absence of a dedicated viral oncogene.
Let's look at the given options based on this understanding:
They cannot activate nearby cellular proto-oncogenes after integration into the genome of the host cell
This is incorrect. Slow-acting retroviruses *do* cause cancer precisely by activating nearby cellular proto-oncogenes through insertional mutagenesis.
They lack an oncogene
This is correct. Slow-acting retroviruses are defined by the absence of a viral oncogene in their genome, which is the key difference from transducing retroviruses.
They exclude mouse mammary tumor viruses
This is incorrect. Mouse mammary tumor virus (MMTV) is a classic example of a slow-acting retrovirus that causes tumors by integrating near and activating cellular proto-oncogenes like Wnt-1.
They have acquired mutations during acquisition of an oncogene
This statement better describes the origin of the oncogenes found in *transducing* retroviruses (derived from cellular genes through recombination/mutation), not a characteristic difference of slow-acting viruses.
Therefore, the primary difference in the genome of slow-acting retroviruses compared to transducing viruses is that slow-acting viruses lack an oncogene.
Listeria is a food-borne pathogen that causes mild gastro-intestinal symptoms. To move from one host-cell to another, it polymerizes actin into a comet tail like structure. Listeria can assemble host-cell actin at its rear end because:
A. Listeria has on its surface a protein called ActA
B. Listeria can activate Arp 2/3 complex
C. Listeria has on its surface γ-tubulin
D. Listeria has on its surface myosin II motor
Which one of the following options represents all correct statements?
Which one of the following plant pathogens has largest genome size?
Pathogens continuously evolve strategies to evade host immune responses. For each of the following evasion strategies (listed in column X) match the pathogen (listed in column Y) which adopts it:
| Column X | Column Y | ||
| A | Changing the antigen expressed on their surface | (i) | Influenza virus |
| B | Increasing phagocytic activity of macrophage | (ii) | Neisseria |
| C | Developing resistance to complement-mediated lysis | (iii) | Gram +ve bacteria |
| D | Secreting proteases to inactivate antibodies | (iv) | No bacteria |
| E | Allowing point mutations in surface epitopes resulting in antigenic drift | ||
PR proteins play important role during plant-pathogen interactions. Column X represents some of the PR family proteins and column Y represents their main properties.
| Column X | Column Y | ||
| A | PR - 2 | (i) | Defensin |
| B | PR - 5 | (ii) | Thaumatin-like |
| C | PR - 12 | (iii) | Lipid transfer protein |
| D | PR - 14 | (iv) | β-1, 3 - glucanase |
Which of the following phytopathogens has predominantly necrotrophic mode of colonization?