Hello {{First Name|there}}, 

Recent reports of hantavirus cases have sparked public attention around a virus many people have never heard of before.

Social media speculation may have led you to question whether the Andes strain of hantavirus could become “the next pandemic.”

However, infectious disease experts and global health agencies emphasize an important distinction:

→ Hantaviruses are serious viral illnesses, but they do not spread with the efficiency of SARS-CoV-2. Human-to-human transmission remains rare and requires prolonged close contact.

A 2014 review published in Viruses examined how pathogenic hantaviruses interact with endothelial cells and angiogenic signaling pathways.

Most hantaviruses spread through exposure to infected rodent urine, saliva, or droppings.

The Andes virus (ANDV), found in South America, is unusual because limited person-to-person transmission has been documented.

Even so, public health experts note several key differences from pandemic respiratory viruses:

→ The World Health Organization currently assesses the broader public risk as low.

Many viruses directly infect and destroy tissues, but hantaviruses infect endothelial cells, the specialized cells lining blood vessels.

These cells regulate:

Research suggests that severe disease develops not only from viral infection itself, but from dysregulation of the signaling pathways that maintain vascular integrity.

One of the most important findings involves the interaction between:

The Andes virus (ANDV), increases endothelial sensitivity to VEGF, a major regulator of vascular permeability and angiogenesis.

Under hypoxic conditions, infected endothelial cells became significantly more permeable, contributing to fluid leakage across the vascular barrier.

Importantly, the virus itself does not appear to directly destroy blood vessels.

→ Instead, it dysregulates the signaling systems that normally control vascular function.

Hantaviruses evade early antiviral immune responses.

Researchers found that pathogenic strains can suppress early interferon (IFN) signaling within endothelial cells, allowing more efficient viral replication.

In contrast, nonpathogenic hantaviruses failed to suppress these responses and showed limited replication in human endothelial cells.

→ This suggests that viral virulence may depend, in part, on the ability to manipulate host signaling pathways.

One hallmark of HPS is rapid pulmonary edema, the accumulation of fluid in the lungs.

This may result from a combination of:

Researchers also identified involvement of the mTOR signaling pathway, which may contribute to abnormal endothelial responses during infection.

This research highlights an important concept in vascular biology:

Many disease are not caused solely by cell death, but by altered signaling within the vascular system

→ Hantaviruses provide a striking example of how disruption of endothelial signaling, angiogenic pathways, and vascular permeability can drive severe disease.

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Best wishes,
- The Angiogenesis Foundation

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