Question

Which of the following neisserial virulence factors is subject to high- frequency antigenic variation by a mechanism involving recombination between silent and expressed chromosomal loci? A. Lipooligosaccharide B. Capsule C. Porin D. Pilin E. Opacity proteins

Short answer

The neisserial virulence factor subject to high-frequency antigenic variation by a mechanism involving recombination between silent and expressed chromosomal loci is Pilin (Choice D).

Step-by-step solution

Understanding the Question

The question is asking which Neisseria's virulence factor changes frequently due to recombination between silent and expressed chromosomal loci. Neisseria is a type of bacteria that has several virulence factors, which are molecules produced to help the bacteria cause disease. These factors undergo changes, known as antigenic variation, to evade the host's immune response.

Elimination of Incorrect Answers

Looking at the options, we can eliminate choices (A) lipooligosaccharide and (B) capsule since they are not primarily known to undergo antigenic variation. Similarly, porin (C) and opacity proteins (E) are not the most frequently changing factors due to this particular mechanism.

Selection of the Correct Answer

The correct answer is (D) Pilin. Pilin proteins in Neisseria exhibit high-frequency antigenic variation, which allows the bacteria to evade the host's immune system. The mechanism behind this antigenic variation involves recombination between silent and expressed chromosomal loci, allowing the bacteria to generate an array of varying pilus structures.

Key concepts

Antigenic Variation

Antigenic variation is a clever survival strategy used by some pathogens, including Neisseria bacteria, to evade the host's immune system. This process involves changes in the surface proteins of the bacteria, which are the targets of the host's immune response.

Think of it as a shape-shifter in a game of tag; the bacteria continuously change their 'appearance' to avoid being 'tagged' or recognized by the immune cells. This change isn't random; it's driven by specific genetic mechanisms such as chromosomal recombination, which allows the exchange of DNA sequences between different regions of the genome. This recombination leads to variations in proteins like pilin, helping the bacteria to persist in their host for longer periods and often causing a chronic infection.

Pilin

Pilin is like the handy tool a spy uses to change disguises. It's a component of the pilus, which is a slender, hair-like appendage found on the surface of Neisseria bacteria. The pilus helps bacteria to adhere to host cells and can be critical for establishing an infection.

Pilins are the building blocks of this structure and due to their presence at the surface, they are subject to the host immune system's surveillance. To dodge this defense mechanism, Neisseria species frequently change the composition of pilin through antigenic variation. This ensures the bacteria can remain undetected, much like how a spy would change outfits to remain undercover.

Neisseria Bacteria

The Neisseria genus encompasses a number of bacteria species, such as Neisseria meningitidis, which causes meningitis, and Neisseria gonorrhoeae, which causes gonorrhea. These bacteria are known for their ability to adapt and survive in their human host, largely due to their arsenal of virulence factors, including the ability to undergo antigenic variation.

They are quite adept at the art of deception when faced with the human immune system. By altering their surface structures, they can continue their infectious cycle and pose a significant challenge for vaccine development. Despite this, vaccines have been developed that target stable components of these bacteria, providing protection against some of the diseases they cause.

Chromosomal Recombination

Chromosomal recombination is a dance of genetic material, an intricate step that leads to genetic diversity. In the context of Neisseria's virulence, it plays a key role in antigenic variation. Recombination is the process of breaking and rejoining DNA strands, allowing genes from different parts of the chromosome to be shuffled and combined.

This genetic mixing can result in new combinations of genes that encode for pilin proteins, leading to different versions of the pilus on the surface of the bacteria. These variations can be so significant that the immune system no longer recognizes the bacteria, even though it has encountered them before. This clever strategy is one reason why developing a broad-acting vaccine against certain Neisseria infections has been challenging.