Cholera bacteria, in their relentless battle for survival, face not only the challenge of antibiotics and public health interventions but also a formidable opponent in the form of bacteriophages (phages) – viruses that prey on and destroy bacteria. These phages play a crucial role in shaping the course of cholera outbreaks, influencing the scale and duration of epidemics.
Since the 1960s, the ongoing 7th cholera pandemic has been fueled by specific strains known as “seventh pandemic El Tor
” (7PET) strains of Vibrio cholerae, which have spread globally in successive waves. In this evolutionary arms race between bacteria and phages, V. cholerae has developed defense mechanisms to combat these viral invaders. Many bacterial strains have evolved to carry genetic elements that equip them with anti-viral tools.
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Why are certain cholera strains so adept at evading phage attacks?
” This question lingers as researchers strive to understand how these interactions contribute to the severity of cholera outbreaks among human populations. An intriguing event that stands out is the devastating cholera epidemic that ravaged Peru and Latin America in the early 1990s, infecting over a million people and claiming thousands of lives. The culprit behind this catastrophic outbreak was identified as strains belonging to the West African South American (WASA) lineage of V. cholerae.
A recent study led by Melanie Blokesch’s group at EPFL’s Global Health Institute shed light on one key aspect that enabled these WASA strains to cause such widespread devastation in Latin America. Published in Nature Microbiology, their research revealed that the WASA lineage had acquired multiple distinct bacterial immune systems that shielded it from various types of phages – a defense mechanism believed to have amplified the scale of the epidemic.
The Peruvian strains from the 1990s were found to be resistant to key phages such as ICP1, a dominant virus known for its role in restricting cholera outbreaks in Bangladesh. By examining these strains’ genetic makeup and conducting experiments where specific genes were transferred between bacterial strains for testing purposes, researchers pinpointed two critical defense regions within WASA strain’s genome: WASA-1 prophage and Vibrio seventh pandemic island II (VSP-II). These genomic regions encode specialized anti-phage systems working together to create a robust bacterial immune response against phage infections.
One noteworthy system identified was WonAB, triggering an “
abortive infection
” response that sacrifices infected cells before phages can replicate fully – essentially saving most bacteria while eliminating a few casualties. Unlike traditional bacterial immune responses like restriction-modification systems which degrade phage DNA upon entry into cells, WonAB halts replication after hijacking cellular machinery without allowing further spread.
David Adams, lead author of the study highlighted how this strategy functions: “
It stops replication after hijacking cellular machinery but prevents further spread.” Additionally, GrwAB targets chemically modified DNA used by some phages for evasion while Vc SduA defends against different virus families including common vibriophages – collectively expanding protection range within bacterial populations.
The WASA lineage’s arsenal encompasses diverse anti-phage defenses beyond immunity against major predators like ICP1 – indicating an ability to counteract various bacteriophages effectively. Understanding how epidemic bacteria evade phage threats is pivotal amidst growing interest in phage therapy as an alternative treatment for bacterial infections.
If pathogens like V. cholerae can enhance transmission potential through acquiring viral defenses,
it could revolutionize approaches towards controlling and treating cholera outbreaks; highlighting significance
of studying intricate dynamics between phages and bacteria during infectious disease management.
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