Abstract
Viruses are obligate intracellular parasites that alter many cellular processes to create an environment optimal for viral replication. Reprogramming of cellular metabolism is an important, yet underappreciated feature of many viral infections, as this ensures that the energy and substrates required for viral replication are available in abundance. Human adenovirus (HAdV), which is the focus of this review, is a small DNA tumor virus that reprograms cellular metabolism in a variety of ways. It is well known that HAdV infection increases glucose uptake and fermentation to lactate in a manner resembling the Warburg effect observed in many cancer cells. However, HAdV infection induces many other metabolic changes. In this review, we integrate the findings from a variety of proteomic and transcriptomic studies to understand the subtleties of metabolite and metabolic pathway control during HAdV infection. We review how the E4ORF1 protein of HAdV enacts some of these changes and summarize evidence for reprogramming of cellular metabolism by the viral E1A protein. Therapies targeting altered metabolism are emerging as cancer treatments, and similar targeting of aberrant components of virally reprogrammed metabolism could have clinical antiviral applications.
Highlights
This review focuses on the alterations made by Human adenovirus (HAdV) to host cell metabolism
In the diet-induced model of obesity, mice transduced with HAdVD-36 E4ORF1 had an upregulation of the glycolytic genes in the liver (Supplementary Table S2) [78]
The changes in cellular metabolism enacted by HAdV infection very closely mimic the metabolic phenotype of cancer cells
Summary
As such, they are critically dependent upon energy and substrates obtained from the infected host cell. HAdVs generally cause acute, lytic infections with a replicative cycle of typically several days between exposure and production of new viruses in quiescent epithelial cells. Viral replication requires the substrates and energy provided by the host cell, and an optimized environment within the virus infected cell ensures maximal HAdV progeny production. The products from the E2 transcription units are primarily involved in viral DNA replication [3]. The E4 transcription unit is comprised of 7 open reading frames (ORFs), the products of which act to modulate cellular function and assist with viral DNA replication and RNA processing [5].
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