Uncovering the Connection: How Atopic Dermatitis Increases Dengue Fever Risk

Uncovering the Connection: How Atopic Dermatitis Increases Dengue Fever Risk

November 27, 2024 Catherine Williams - Chief Editor Health

Dengue Disease Overview

Dengue is caused by the dengue virus and spread by mosquitoes, specifically Aedes aegypti and Aedes albopictus. It has four serotypes: DENV1, DENV2, DENV3, and DENV4. Dengue is a global health problem, endemic in over 100 countries. The incidence and geographical spread of dengue have increased significantly in recent decades. The World Health Organization (WHO) estimates that 50 million people are infected with the dengue virus each year, resulting in approximately 25,000 deaths. The clinical manifestations of dengue vary widely, ranging from no symptoms to severe cases involving plasma leakage, bleeding, and even death.

Immune Response Mechanisms in Dengue

The initial immune response to dengue begins when the virus enters the body through mosquito bites, targeting dendritic cells (DCs), macrophages, and Langerhans cells (LCs) in the skin. After entering these cells, the virus replicates. The immune system recognizes the viral presence, triggering the production of interferons (IFNs), which create an antiviral environment. This signals other immune cells to join the fight against the virus. Natural killer (NK) cells play a role in destroying infected cells.

However, the dengue virus has mechanisms to evade the immune system, allowing for viral persistence and replication. In patients with atopic dermatitis (AD), there are notable changes in immune response. DCs and macrophages are more abundant in lesional and non-lesional skin, creating an environment conducive to viral replication. This is exacerbated by skin barrier defects characteristic of AD, which allow allergens and pathogens to penetrate more easily.

Immune Dysregulation in Atopic Dermatitis

In people with moderate to severe AD, several immune cells, including mast cells (MCs) and innate lymphoid cells (ILC2s), respond to the presence of dengue. Increased levels of cytokines like IL4 and IL13 activate DCs and macrophages, making them more permissive to the dengue virus. Additionally, MCs release chemicals that increase blood vessel permeability, facilitating the entry of more immune cells to the infection site, yet this can result in worsened inflammation and severe dengue.

The balance between various immune responses is disrupted in AD. While there is often an increase in Th2 cytokines, Th1 responses, which could help control the virus, are weakened. This imbalance can lead to higher risks of dengue infections in AD patients.

Clinical Implications

The increased presence of DCs, M2 macrophages, and mast cells in the skin of AD patients means that these individuals may have a greater susceptibility to dengue virus infections. The combination of immune dysregulation and alterations in immune cell function facilitates dengue viral entry and replication. This understanding underscores the importance of monitoring AD patients closely for potential dengue infections and adjusting their management as needed to mitigate risks.

Conclusion

Dengue is an infectious disease with increasing prevalence. The compromised skin barrier in people with AD and their altered immune responses can enhance the risk of severe dengue. Ongoing research is crucial to understand better the link between AD and dengue infection, informing clinical practices and preventive strategies.