Naturally found in South East Asia, accidental introductions led to invasive populations of C. parasitica in North America and Europe.

In the first half of the 20th century, the fungal disease had a devastating economic and social impact on communities in the eastern United States.

[4] CHV1 is one of at least two viral pathogens that weaken the fungus through hypovirulence and helps trees survive a blight infection.

The European chestnut (Castanea sativa) is also susceptible, but due to widespread CHV1 hypovirulence, blight-induced tree death is less common.

[7] The fungus can infect other tree species such as oaks, red maples, staghorn sumacs, and shagbark hickories.

Fungal strains spread by wind-borne ascospores and, over a shorter distance, conidia distributed by rain-splash action.

However, these regrown shoots seldom reach the sexually reproductive stage before above ground growth is again girdled by the fungus.

Cryphonectria parasitica was introduced into the United States from East Asia via import of Japanese chestnut trees.

[28] Hypovirulence is not widespread in the US and attempts to commercially introduce CHV1 virus have not been widely successful [citation needed].

Due to genetic differences between the fungal populations (strains), it is likely that a second introduction of chestnut blight occurred in Georgia and Azerbaijan in 1938.

[citation needed] The fungus enters through wounds on susceptible trees and grows in and beneath the bark, eventually killing the cambium all the way around the twig, branch, or trunk.

This acid lowers the pH of the infected tissue from around the normal 5.5 to approximately 2.8, which is toxic to cambium cells.

If cankers continue to form and expand, the fungus can girdle the stem, severing the flow of nutrients and water to the vital vegetative tissues.

In Europe, during the late 1960s, it was found that a strain of C. parasitica was less virulent, only able to produce shallow cankers that the tree's callus tissue could eventually limit and isolate.

In Europe, natural dissemination of hypovirulence in pathogen populations resulted in the restoration of economically valuable chestnuts.

Sanitation practices like the pruning of symptomatic limbs and removal of infected trees can serve to eliminate sources of inoculum and limit the spread of the pathogen.

A study on the chemical control of chestnut blight in Castanea sativa, may have found that the external application of both copper oxychloride and carbendazim could reduce the rate of disease by almost 50%.

[40] Current efforts are underway by the Forest Health Initiative to use modern breeding techniques and genetic engineering to create resistant tree strains, with contributions from SUNY College of Environmental Science and Forestry, Pennsylvania State University, the University of Georgia, and the United States Forest Service.

One of the most successful methods of breeding is to create a back cross of a resistant species (such as one from China or Japan) and American chestnut.

The strategy is to select blight-resistance genes during the backcrossing while preserving the more wild-type traits of American chestnut as the dominant phenotype.

A 1983 study on hypovirulence had shown that chestnut blight infected with hypovirus produced less oxalic acid when attacking the cambium.

[43][44] Meanwhile, a plant pathologist, Dr. William Powell, had been trying to figure out how to transfer all of the Asian chestnut's resistance genetics to its American relatives.

[45] (In related work, in 2001 Liang, Mayard, Allen, and Powell successfully inserted an oxalate oxidase (OxO) gene from wheat into Populus × euramericana ("Ogy") for Septoria musiva resistance.

[46] This enzyme breaks down the oxalic acid secreted by the fungus into carbon dioxide and hydrogen peroxide.)

In 2007, Welch, Stipanovic, Maynard, and Powell showed that transgenic C. dentata expressing a wheat OxO indeed had lower lignin degradation by oxalic acid, and suggested this was the path to take.

[47][44] A few years later this line of research culminated in the final product: Powell[48][49][50] and another plant pathologist, Dr. Charles Maynard, working at the State University of New York College of Environmental Science and Forestry developed American chestnuts which had heightened blight resistance.

[49] Powell's lab had been able to use growth chambers with higher light inputs to get duration to pollen production down to less than a year.

[56] However, in December 2023, TACF withdrew its petition for use as a restorative species due to poor performance and high mortality in Darling 54 saplings.

[57] In less than fifty years after its emergence, C. parasitica virtually eliminated American chestnut as a canopy species in 8.8 million acres (3.6×10^6 ha) of forest.

[58] Therefore, in addition to ecological impacts, C. parasitica potentially caused a devastating loss in economic welfare for communities dependent on the chestnut tree.