In short, our data shows the best immune response for SARS-CoV-2 is found from the COVID-19 vaccine alone. However, giving flu and COVID-19 vaccines together produces strong responses to both viruses.

These findings can help guide vaccine administration strategies and inform the public of impacts of both vaccine timing and placement for the upcoming viral infection season.

It was previously thought that immunity from mRNA COVID-19 vaccines fades away quickly, but our study shows that it lasts a long time and stabilizes over time. 

Booster shots helped to level out the antibody responses in people, whether they had previous immunity or not. 

When looking at how antibody levels change over time, there are two phases: a rapid rise and then drop-off at first, followed by a period where antibody levels remain stable.

There are some coronaviruses that cause common colds, however becoming sick with these viruses does not give you much protection against other coronaviruses.

Currently, people who have been infected with or vaccinated against COVID-19 have antibodies that can react to a wider variety of coronaviruses – providing greater protection. So, our bodies are now primed to recognize and fight off a broader range of coronaviruses.

It's not yet clear if these antibodies protect us from getting sick with new coronaviruses, but it could mean we are better prepared for future coronavirus threats.

This study looked at how many people in New York City between 2020-2023 had antibodies against the COVID-19 virus in their blood, which shows if someone was previously infected or vaccinated.

By mid-2022, a large majority (over 90%) of people in the study had antibodies to the COVID-19 virus.

Ultimately, we illustrated how immunity changed in a large metropolitan area during the COVID-19 pandemic.

This paper looked at how well the bivalent COVID-19 vaccine worked in patients with Multiple Myeloma (MM), a type of cancer that weakens the immune system. 

The study found that the bivalent vaccine does improve protection against the Omicron variant in these patients. However, the patients were still vulnerable to newer COVID-19 variants. 

In essence, while the bivalent vaccine offers some benefit to MM patients, its effectiveness can be limited by specific treatments that weaken the immune system.

Interferons are important substances in the body that fight viruses and cause inflammation.

They trigger the production of other substances called interferon stimulated genes (ISGs). ISG15 is one of these ISGs.

Even if people do not have enough ISG15, they can still resist viral infections because they have high levels of other ISGs.

Our study showed that cells lacking ISG15 are more resistant to HIV-1 infection. This resistance is related to specific ISGs found in T cells.

In this paper, we studied how a protein called IL-15 affects the infection of specific immune cells (CD4+ T cells) by HIV and found that IL-15 causes changes in these immune cells that make them more susceptible to HIV infection. 

We also identified a key step in this process involving a protein called JAK.

Our study suggests that blocking JAK could be a way to help prevent HIV from establishing a long-term infection in the body.

Viruses must be able to navigate the cells they infect, using the cell's own machinery to replicate while also fighting off the cell's defenses. 

HIV uses specific proteins to counteract the cell's defenses. These proteins help scientists understand how HIV evolves and how to develop new treatments. 

The paper focuses on how HIV fights against three specific defense mechanisms: APOBEC3, SAMHD1, and tetherin.

Our bodies have natural defenses against HIV. One defense is a protein called A3H.

A3H can stop HIV from making copies of itself. However, there are different forms of A3H, and some are better at this job than others.

This study looked at how HIV changes to overcome A3H. These changes help HIV to keep replicating. This research highlights the ongoing battle between our bodies and HIV, and how the virus evolves to survive.

All human genomes contain sequences belonging to old viruses called Human Endogenous Retroviruses (HERVs). The most ancient HERVs are estimated to be 60-70 million years old.

Usually, these HERVs are inactive, but in diseases like cancer, they can turn back on.

Their specific expression provides the opportunity to use HERV proteins as biomarkers and possible targets for immunotherapy.

We used a new strategy to study the HERV-K HML-2 group and figure out which ones are making proteins.  

Just measuring the RNA levels of HERVs isn't enough to know which ones are producing proteins.  

Our new approach combines different lab techniques to precisely identify which HERV-K HML-2 elements are active.  

We tested this methodology on a cell line that produces HERV-K proteins and were able to pinpoint exactly which HERV-K elements were responsible.

In essence, we developed a more accurate tool to study active HERVs and showed how it can give us a clearer picture compared to older methods.

This paper explains how HIV-1 infection affects the activity of certain ancient virus remnants, called HERV-K (HML-2), found in our DNA, specifically in CD4+ T cells (a type of immune cell).

Our "Inner Viruses": Our genome contains mainly inactive fragments of old viruses called ERVs. Most are harmless, but some, like HERV-K (HML-2), can still "wake up" and produce viral RNA and proteins. Their activity is usually strictly controlled, but diseases such as HIV can change this.

Old Problem, New Solution: Because these HERV-Ks (HML-2) are encoded by very similar DNA sequences, it's been hard to study exactly which ones are active. We used a new, very precise sequencing method to identify specific HERV-K (HML-2) elements that become active in HIV-infected cells.

HIV's Influence: While HIV-1 didn't change the overall amount of HERV-K (HML-2) activity, it did affect specific ones:

Three particular HERV-K (HML-2) elements became more active (increased by 3 to 5 times) in HIV-infected cells.

One specific HERV-K (HML-2) element actually became less active when HIV was actively multiplying.

Why It Matters: This study identifies which specific HERV-K (HML-2) elements are impacted by HIV. This is important for future research to understand if these ancient viruses play a role in how HIV progresses and if they could be new targets for treatments. It also suggests that previous ideas about HIV and HERV-K might be more complex and depend on other factors in the body.

In short, the paper shows that HIV infection doesn't just impact immune cells; it also subtly changes the activity of specific "fossil viruses" within our own genes.

This paper is about how a specific protein from an ancient human virus, called HERV-K108 Env, can stop the AIDS virus (HIV-1) from making more copies of itself.

HERV-K's Impact on HIV-1: We discovered that a protein called "Env" from some types of Human Endogenous Retrovirus (HERV) especially HERV-K108, significantly reduced how much HIV-1 could produce.

Broad Inhibition: This effect wasn't just on one type of HIV-1; it worked against various lab-grown and real-world strains of HIV-1. It also affected other similar viruses like HIV-2 and SIVs, though some were more resistant than others.

How it Doesn't Work: The HERV-K108 Env protein doesn't stop HIV-1 by inhibiting its RNA synthesis (transcription) or by generally harming the cell's ability to make proteins. It's also not due to another HERV-K protein called Rec.

Key Charcteristics: The researchers found four specific differences (amino acids) in the HERV-K108 Env protein that are essential for it to block HIV-1 production.

Protection: This research suggests that some of these ancient human viruses within our own DNA might have a natural ability to fight newer viruses like HIV-1. More studies are needed to figure out how to harness the production of these protective HERV proteins.