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You can check out Dr. Gerald’s latest COVID Epidemiological Review Here. The Appendix this week has an informative county by county epidemiological analysis. Summary of Dr. Gerald’s report is below, but make sure to view the full report– there are lots of interesting figures in the report this week.

• Arizona is transitioning to a new phase of the outbreak where viral transmission is declining in the working-age and older adult populations but beginning to increase among adolescents and young adults. This is most likely attributable to re-opening of university campuses.

o Rising cases on university campuses pose an unknown risk to the broader community as it is unclear to what extent that the social networks of students and the broader community overlap.

o While the risk of severe disease in young adults is low, that is not the same as no risk. As case counts increase, some young adults will invariably require hospitalization and it is not out-of-the question that a small number of deaths could result.

o Reporting lag for PCR results has improved such that ≥90% of results are returned within 48 hours; however, the rapid rise in antigen testing on University campuses may present new challenges in data reporting and interpretation.

• Outside of young adults, levels of community-driven viral transmission remain comparatively high but continue to decline. Overall, transmission levels are on par with those observed in late-May.

o For all locales, mask-wearing ordinances will be needed for the foreseeable future to mitigate the spread of Covid-19.

o As some additional business activities (e.g., schools and businesses) resume, they will bring more people into closer contact and will facilitate additional viral transmission. Therefore, continued adherence with mask wearing, physical distancing, hand hygiene, and surface decontamination will be needed to mitigate these risks.

• Covid-related hospital utilization continues to decline while excess capacity is not being replenished owing to larger amounts of non-Covid care. However, adequate capacity is available for the foreseeable future.

o From now until January, non-Covid hospitalizations are expected to increase putting additional strain on hospital capacity.

o Hospitals will continue to experience large volumes of elective care to address the backlog of patients waiting elective procedures.

• Current Covid-19 test capacity appears adequate as evidenced by quick turn-around for PCR results and a PCR test positive percentage of 5% which is within the recommended 3 – 5% threshold.

o As more Covid-19 testing transitions to antigen testing, it is unclear how this might impact test positivity trends. A rising test positive percentage should raise the possibility of resurgence.

County Data (weekly crude and population-adjusted cases counts) appear in Appendix.

Next update scheduled for September 11.

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CMS announced regulatory changes that require nursing homes to test staff and offer testing to residents for COVID-19. Laboratories and nursing homes using point-of-care testing devices will now be required to report diagnostic test results. The new rules also require hospitals to provide COVID-19 cases and related data to HHS.

This is a welcome intervention that will help save lives and protect valuable hospital capacity this fall and winter. It only applies to skilled nursing facilities that are certified by CMS (because Medicaid or Medicare is a payer for some of the residents). It wont help with Assisted Living centers or homes because those aren’t CMS certified.

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Join Us!

If somebody forwards this Weekly Public Health Policy Update to you & you’re interested in getting them every week – please join AzPHA!

You can join us at on our membership web link. Individual memberships are only $75/year and student memberships priced at just $25/year. 

We also have various Organizational Memberships.

Part II: What About the Long Run, Is there Lasting Immunity?

Once the immune system is successful at fighting off a threat like the SARS CoV2 virus it can begin to relax.  Because the antigen is no longer around after a person finally recovers, there’s no need to continue to mount the immune response. The immune system keeps some antibodies around for a while just in case the person is exposed to the virus again. If that does happen, then the antibodies (IgG), are at the ready and can neutralize the virus right away and draw in a few phagocytes to kill the virus before it replicates.

After a couple of years have passed and the body hasn’t seen the virus around, it often begins to stop making those antibodies. But it has a memory.  Even if all the antibodies are gone from the blood, the immune system will remember that virus- even decades later in some cases. 

The B Cells that make the antibodies stand at the ready to make new antibodies right away and they won’t have the learning curve like they had the first time. Likewise, the T cells that specialized in attaching the virus will be at the ready.  Even when those original B and T cells eventually die- their offspring still remember the old virus and can ramp up fast.

Will People that Recover have Lasting Immunity? All indications are yes. An article recently published in the highly respected journal Nature found that patients who had recovered from COVID-19 mounted a full immune response that included the production of antibodies (via B cells), complement fixing, while blood cell production (phagocytes) and a robust T cell response.

This is an important finding that informs whether people that have recovered from a COVID-19 infection are protected from additional infections. The data in this study strongly suggest that the answer to that question is “yes, there is lasting immunity”.

Indeed, even after antibody production (titer) wanes after a period of months or years, the evidence suggests that memory B cells will be around to produce antibodies quickly if needed.  In addition, the study shows that specific T cells with memory will also be around to mount a specific response to a future exposure to the virus.

A separate study published in the British Medical Journal found that “recovered individuals developed SARS-CoV-2-specific IgG antibody and neutralizing plasma, as well as virus-specific memory B and T cells that not only persisted, but in some cases increased numerically over three months following symptom onset.  These findings demonstrate that mild COVID-19 elicits memory lymphocytes that persist and display functional hallmarks associated with antiviral protective immunity.”

Part I – Antibodies, Leukocytes & T Cells

Over the last several months we’ve learned a lot about the nature of the immune response when someone is sick with and then recovers from a SARS CoV2 infection. At first, it was unclear whether and for how long immunity might last after recovery. Most of the public and media discussion has been about the lasting effect of neutralizing antibodies following recovery from COVID-19….  but the immune system is so much more than just an antibody response.

This week I’m doing my best to explain the basics of the immune system, how it works and it’s different components.

What Is the Immune System?

The immune system is the body’s defense against infections from pathogens like bacteria and viruses. It consists of a combination of different kinds of cells that attack pathogens to keep us healthy. Our immune system can detect different kinds of disease agents and it’s really good at telling the difference between harmful and harmless or even beneficial organisms (e.g. viruses, bacteria, and parasites).  It can tell the difference between the body’s own healthy cells or tissues, and ‘foreign’ cells.

When the immune system recognizes a pathogen (let’s take the SARS CoV2 virus as an example) it activates the immune system to protect the host. That immune response starts with intelligence gathering.

Intelligence Gathering

The immune system’s “intelligence gatherers” are called B lymphocytes.  You might also know them as Bursa cells. These cells go around the body all the time and look for foreign objects that could be harmful. They’re looking for “antigens” or proteins that look strange and potentially harmful.

For example, the SARS CoV2 virus that causes COVID-19 has a has a protein coat that is unique to that virus. The antigens, or protein coat spikes are those sharp looking things that are often depicted in the media when they show the virus. The immune system’s B cells brush up against the virus and gather intelligence- and when they see the SARS CoV2 virus, they immediately think uh-oh.  This is not good. Let’s make some antibodies to fight this antigen.

Emergency Response

Those antibodies are the “first responders” of the immune system. You can think of antibodies as firefighters that rush in to fight the threat that the invading virus may be posing. The B lymphocytes (B Cells) make the antibodies (also called immunoglobulins).  They are proteins that lock onto the specific antigen that’s the threat. 

You can think of it like a lock and key. The key needs to fit the lock to open the door. It’s like that, the antibody needs to fit the antigen to work too. When the key and the lock fit- the harmful virus becomes neutralized. Not dead, but neutralized.

There are several different kinds of antibodies. Two of the most important at IgM and IgG. Both are antibodies, but they have slightly different purposes. The IgM antibodies produced by the B cells form first, within the first couple days after infection. They do an OK job, but they aren’t super effective- but they can be made really fast. IgG antibodies take longer to make but do a better job once they get there.

Antibodies lock on to the threat and neutralize it, but they can’t kill the virus without help. The antibodies put handcuffs on the virus so that it’s held in abeyance until assistance arrives.  The first help to arrive is a group of proteins called “complement”.

The complement arrives and sees that an antibody has locked on to the SARS virus.  Complement triggers a chemical reaction that damages or kills the viruses, infected cells and other close by cells that are healthy. The complement is a pretty blunt immune system instrument because it kills both the virus, infected cells and other cells that aren’t infected. 

But more help is on the way.  They’re called “phagocytes”.

Calling in the Cavalry

Phagocytes are immune system cells that “eat” harmful foreign particles, bacteria, as well as dead or dying cells. These cells come to the rescue when they see that antibodies have been neutralizing harmful pathogens and causing a complement response. These “professional” phagocytes include a host of different white blood cells called neutrophils, monocytes, macrophages and dendritic cells.

These cells act to kill the invading organism, but it comes at a cost, because healthy host bystander cells are destroyed as the phagocytes react to the threat.  The macrophages and neutrophils for example cause an inflammatory response that damages healthy host tissue. They destroy pathogens by engulfing them and subjecting them to toxic chemicals. 

Sometimes those toxic chemicals are released into the environment causing the damage to healthy host cells. This process helps the body get rid of the harmful invaders but also causes inflammation to normal healthy cells that are bystanders.

Bringing in the Specialists

The immune system specialists are the T Cells.  They provide an important role in controlling and shaping the overall long-term immune response.  They use signaling proteins called cytokines to recruit to mount an immune response. Other kinds of T cells are called “helper cells” which indirectly kill foreign cells by attracting phagocytes.

The T cells learn to specifically target the harmful invaders and can attack those invading virus and bacteria in a targeted way that causes less collateral damage to the surrounding tissue. They can also recognize, target, and destroy things like cancer cells. 

People spend their whole career studying T cells and their function in the immune system- so their work is complex and important.

Part II Tomorrow: Is there Lasting Immunity Post Infection?