Ticks are tiny arachnids that feed on the blood of animals and humans. They can also transmit various diseases, such as Lyme disease, Rocky Mountain spotted fever, and anaplasmosis.
Anaplasmosis is a bacterial infection that causes fever, headache, chills, muscle aches, and sometimes severe complications.
It is caused by a bacterium called Anaplasma phagocytophilum, which is transmitted by the black-legged tick and the western black-legged tick.
In the United States, the number of anaplasmosis cases has increased from 348 in 2000 to 5,655 in 2019.
How does Anaplasma phagocytophilum infect ticks and humans?
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Anaplasma phagocytophilum is a zoonotic agent, meaning it can infect both animals and humans. It mainly infects white blood cells called neutrophils, which are important for fighting infections.
When a tick bites an infected animal, such as a deer or a mouse, it picks up the bacteria and carries them in its gut.
The bacteria then need to cross the gut barrier and reach the salivary glands of the tick, where they can multiply and wait for the next host.
When the tick bites another animal or a human, it injects the bacteria into the bloodstream along with its saliva.
To achieve this complex life cycle, Anaplasma phagocytophilum has evolved various strategies to evade and manipulate the immune system of both ticks and mammals.
One of these strategies involves secreting proteins that can interact with and modify the host cells.
These proteins are called effectors, and they can alter the host cell's structure, function, signaling, and gene expression to favor the survival and spread of the bacteria.
How does AteA help Anaplasma phagocytophilum survive in ticks?
A recent study led by researchers at Washington State University has identified one of these effectors, called AteA, that is essential for Anaplasma phagocytophilum's survival and propagation in tick cells.
The researchers used genetic engineering to create mutant strains of the bacteria that lacked AteA or had a modified version of it.
They then infected tick cells with these strains and observed their growth and behavior.
They found that AteA is secreted by the bacteria and injected into the tick cell's cytoplasm, where it interacts with a component of the cell's skeleton called cortical actin.
Cortical actin forms a network of filaments under the cell membrane that supports the cell's shape and movement.
AteA binds to cortical actin and changes its organization, which affects the cell's membrane dynamics and endocytosis.
Endocytosis is a process by which cells engulf and internalize molecules or particles from their surroundings.
The researchers hypothesized that AteA helps Anaplasma phagocytophilum enter and exit tick cells by modulating endocytosis.
They also speculated that AteA may protect the bacteria from being degraded by lysosomes, which are organelles that digest foreign material inside cells.
They showed that AteA is required for the bacteria to form large aggregates inside tick cells, which may facilitate their transmission to mammals.
What are the implications of this discovery?
This study is one of the first to unravel the molecular mechanisms by which Anaplasma phagocytophilum persists and spreads within ticks.
It reveals a novel role for AteA as an effector protein that manipulates tick cell biology to benefit the bacteria.
It also provides a new target for developing strategies to prevent or treat anaplasmosis and other tick-borne diseases.
The researchers suggested that blocking AteA or its interaction with cortical actin could impair the bacteria's ability to infect and transmit through ticks.
This could be achieved by designing drugs or vaccines that target AteA or its binding site on actin.
Alternatively, genetic engineering or gene editing could be used to create ticks that are resistant to Anaplasma phagocytophilum infection by disrupting AteA or actin expression.
The researchers also hope that their findings will inspire further research on other effectors secreted by Anaplasma phagocytophilum and other tick-borne pathogens.
Understanding how these effectors function and interact with host cells could reveal new insights into the biology and ecology of ticks and their associated diseases.
