Dissertation defence (Virology): MSc Rickard Lundberg
MSc Rickard Lundberg defends the dissertation in Virology titled “Viral strategies against the interferon system: Mechanisms of innate immune evasion in human coronavirus 229E and Zika virus infection” at the University of Turku on 25 September 2026 at 12.00 (University of Turku, Medisiina D, Alhopuro auditorium, Kiinamyllynkatu 10, Turku).
Opponent: Docent Tero Ahola (University of Helsinki)
Custos: Professor Heli Harvala (University of Turku)
Summary of the Doctoral Dissertation:
How two very different viruses evade and circumvent the body's alarm system
Every time a virus enters a host cell, a race between the cell’s defense system and the virus’s own replication machinery starts. The cell has sensors built in that are supposed to notice when something suspicious, such as the presence of foreign genetic material, is going on and if they notice fast enough, they set off an alarm. That alarm then causes the cell to send out dedicated warning signals, called interferons, that tell neighboring cells to defend themselves and call in the rest of the immune system. If a virus can bypass or find a way to silence this alarm, it buys itself crucial time to replicate.
A new doctoral dissertation from the University of Turku examines two very different viruses and asks how each of them manages that evasion.
The first is human coronavirus 229E, one of four so-called seasonal coronaviruses that are usually associated with the common cold. The second is Zika virus, the mosquito-borne virus behind the 2015-2016 outbreak in the Americas, where it was linked to serious birth defects. While these viruses are unrelated and cause entirely different diseases, they must both overcome the same cellular alarm system to succeed.
For the common cold coronavirus, the research revealed that the alarm barely goes off at all. Infected cells produced large amounts viral progeny, yet the cellular sensors that are supposed to notice virus-associated genetic material failed to detect anything, even when that genetic material was isolated and then artificially introduced into fresh cells. Furthermore, when the infected cells were exposed to a warning signal directly, from the outside, they still mostly failed to generate a response to the infection. This suggests that not only does the virus successfully hide from the cellular defenses, it also carries factors that interact with the cell in such a way that even if the alarm does go off, the cell still seems to lose the ability to respond to the infection properly.
Zika virus takes a more direct approach. Testing each of its proteins one at a time revealed that one protein, called NS5, sharply reduces the alarm signal on its own. The NS5 protein does this, at least in part, by attaching directly to one particular key protein in the alarm-signaling pathway and disabling it, or at least significantly inhibiting its function, cutting off that link before the signal can get through.
The NS5 protein also appears to play a secondary and potentially critical, suppressive function in addition to its interaction with the alarm-associated protein. Instead of remaining in the main cellular compartment where the alarm pathway operates, most of the NS5 protein ends up inside the cell's nucleus, where the cell's genetic instructions are stored. There, it clusters with several key nuclear proteins such as those associated with structures involved in processing of the information carriers of the cell’s genetic material and through that function causing general and systemic dysregulation of the cells overall function and health. While the full impact of this second, nuclear role on cell defense evasion remains to be fully mapped, it indicates that the same single virus protein may be working two jobs inside the cell simultaneously.
While findings like these are not likely to change how a common cold or a Zika virus infection are treated tomorrow, they do provide critical insights into virus stealth strategies. By pinpointing how these relatively simple viruses effectively disarm or circumvent the quite complex cellular defenses, the research provides a precise framework for developing future antiviral therapies designed to block these tricks.
