L'Italo-Americano

THURSDAY, JUNE 25, 2020 www.italoamericano.org 16 L'Italo-Americano C o V i D - 1 9 p a n - d e m i c a s o f 1 9 J u n e 2 0 2 0 : Globally - Con- f i r m e d C a s e s : 8 , 7 3 1 , 7 0 0 + ; F a t a l i t i e s : 461,430+; New cases (24 h): 27,180+ (0.311%)* Italia - Confirmed Cases: 2 3 8 , 0 1 0 + ; F a t a l i t i e s : 34,560+. New cases (24 h): 250+ (0.105%)* US - Confirmed Cases: 2 , 2 9 0 , 8 3 0 + ; F a t a l i t i e s : 121,300+. New cases (24 h): 27,180+ (1.186%)* California - Confirmed Cases: 168,130+; Fatalities: 5,380+. New cases (24 h): 1,120+ (0.667%)* L o s A n g e l e s C o u n t y - Confirmed Cases: 78,240+; F a t a l i t i e s : 3 , 0 2 0 + . N e w cases (24 h): 17 (0.022%)* V i l l a S c a l a b r i n i C o n f i r m e d C a s e s : 8 Residents, 12 Staff (publichealth.lacounty.g ov) * : n e w c a s e s a s % o f total cases – in a situation that is "flat," where infec- tion rates are controlled by p u b l i c h e a l t h m e a s u r e s , increased testing does not result in increased number of cases and the new cases as % of total cases metric falls, and will eventually approach 0.000..% when the infection spread is con- trolled. By contrast, in situ- ations where infection is still rising, the metric of n e w c a s e s a s % o f t o t a l cases rises as well, and can reach 1% and much higher, when the infection is out of control. For example: Arizona: 6.95%; Brazil: 4.8%; Florida: 4.3%; India: 3 . 7 % O k l a h o m a : 3 . 6 % ; Mexico: 3.4%; Texas: 2.8%; Philippines: 2.3%; Russia: 1.4% US: 1.2%; Portugal: 0.97%; California: 0.7%; UK: 0.5%; World: 0.3%; etc. vs. G e r m a n y : 0 . 2 8 % ; Belgium: 0.21%; NY State: 0 . 1 7 % ; N o r w a y : 0 . 1 4 % ; Italy: 0.1%; Spain: 0.1%; L A C o u n t y : 0 . 0 2 % ; W a s h i n g t o n S t a t e : 0.004%; etc. Last December, the first cases of a new pulmonary disease were reported in W u h a n , C h i n a . I n e a r l y January, less than seven months ago, the responsi- ble etiologic agent, the sec- o n d C o r o n a v i r u s o f t h e SARS strain (SARS-Cov2) w a s i d e n t i f i e d a n d sequenced, and the pathol- o g y n a m e d t h e C o r o n a Virus Disease of 2019 (CoViD-19). In the past seven months, CoViD-19 has become a fulminant and deadly pandemic, for which we have no vaccine and no proven treatment, and which we can control only by strict public health measures (i.e., masks and facial covering, and physi- cal distancing; and, when needed, quarantine). As of today, we know a few things about the virus and the pathology it caus- es. We know, for example, that the Spike protein (S) of the virus is what binds to ACE2 receptors on human c e l l s , a n d w e k n o w t h a t then enzymes on the cell membrane clip S, allowing the virus to fuse with the membrane and infect the cell. We know that S is cov- ered with sugar moieties, making it a glycoprotein, against which our immune system has great difficulty in building efficient anti- b o d i e s , w h i c h h a m p e r our ability to develop vaccines. We also know that most of the specific antibodies in convalescent plasma is against the virus nucleocapsid protein, not S, rendering even the use o f c o n v a l e s c e n t p l a s m a somewhat unreliable, or at l e a s t o f u n p r e d i c t a b l e effectiveness. To be clear, w e h e a r r e p o r t a l m o s t every day of this new vac- cine here, that new vaccine there: but de facto, we soon learn that the new antibody species do not bind well to S , a r e n o t s u s t a i n e d i n t i m e , a n d t h e r e f o r e a r e most likely not the ideal candidate for a vaccine. In b r i e f , i t m a y b e s e v e r a l months before we can pro- duce and distribute world- wide an efficient long-last- ing vaccine. We also know a bit about the life cycle of the virus: how its RNA is translated into protein, reverse tran- scribed into DNA for inser- tion into the host genome, a n d h o w i t i s s h e d . Therefore, we are actively working at developing new and improved anti-virals. But the fact of the matter is that we have not yet identi- fied the gold standard anti- v i r a l a g e n t s p e c i f i c f o r SARS-Cov2. With close to nine mil- l i o n c o n f i r m e d c a s e s o f infection world-wide over the past several months, we have gathered a sub- stantial body of evidence with respect to the disease itself. We know the virus causes a widespread spec- trum of pathologies, and several experts are begin- ning to call it a syndrome, a set of diverse pathologies all sharing one common underlying causative agent (cf., HIV causes the human i m m u n o d e f i c i e n c y s y n - drome, AIDS). W h e t h e r w e s p e a k o f CoViD-19 or CoViS-19, the fact remains that, we know, infection with SARS-Cov2 can affect the brain and the central nervous system, the heart and the cardiovascu- lar system, the lungs and pulmonary efficiency, the gastrointestinal tract, the liver and kidneys, as well as c e r t a i n f u n d a m e n t a l p h y s i o - b i o c h e m i c a l processes, including blood c o a g u l a t i o n . M a n y p a t i e n t s , i n d e e d , d i e o f widespread thrombi (i.e., b l o o d c l o t s ) a n d m i c r o - t h r o m b i t h r o u g h o u t t h e body, consequential to the immune response to SARS- Cov2. Perhaps because of the very masked nature of the S p r o t e i n , t h e a n t i - v i r a l i m m u n e r e s p o n s e ( i . e . , cytotoxic T cells) becomes impaired soon after infec- tion – but impaired in a characteristic manner: the cells do not become non- responsive (i.e., anergic), o r d e a d b y n e c r o s i s o r a p o p t o s i s ( i . e . , p r o - g r a m m e d c e l l d e a t h ) , r a t h e r t h e y a p p e a r " e x h a u s t e d . " T c e l l s o f CoViD-19 patients appear to have exhausted their cel- Per Saperne Di Più: CoViD-19, a word with Francesco Chiappelli Issue 7, Dott. Francesco Chiappelli, Prof. emeritus UCLA Center for the Health Sciences l u l a r e n e r g y . Y e t , t h e immune system "sees" this viral infection, and must r e s p o n d . B u t i t n o w responds, if you will, in an u n r e g u l a t e d m a n n e r (because the regulatory T cells are incapacitated). Lots of factors, known as cytokines, are produced. Their role is – under con- t r o l l e d c o n d i t i o n s – t o stimulate and to repress e a c h o t h e r a s n e e d e d t o bring about a balanced cel- l u l a r i m m u n e r e s p o n s e . W h e n t h e i m m u n e response is not regulated (i.e., inactive regulatory T cells), this cytokine release seemly occurs as a never- ending tsunami of sorts, a storm of very potent fac- tors that are very toxic. It is this cytokine storm that afflicts the patients with most severe CoViD-19 by damaging the lungs often beyond repair, by trigger- i n g t h e b l o o d c l o t t i n g responsible for multiple thrombi, and by causing the many other pathologies we see in these patients. E v e n t h e p a t i e n t s w h o recover from SARS-Cov2 infection show long-lasting s i g n s a n d s c a r r i n g f r o m CoViD-19, from structural d e s t r u c t i o n o f t h e l u n g functional architecture, to deficiency of the cardiac muscle, to – most likely, although the evidence is inconclusive at this point – s e r i o u s a n d p e r m a n e n t neurological and cognitive d y s f u n c t i o n s . A l l t h e s e long-lasting sequelae of C o V i D - 1 9 c a n b e t r a c e d b a c k t o t h e d e s t r u c t i v e e f f e c t s o f t h e c y t o k i n e storm. Drs. Horby and Landray and their clinical research collaborators from Oxford U n i v e r s i t y r e a s o n e d months ago that, since one main problem of CoViD-19 is the cytokine storm, per- h a p s b l u n t i n g c y t o k i n e production could decrease CoViD-19 morbidity and mortality. Their reasoning was based largely on the extensive body of research on the immune-regulatory r o l e o f n a t u r a l s t e r o i d s , s u c h a s g l u c o c o r t i c o i d (GC), that stemmed from t h e s e m i n a l w o r k o f P r o f e s s o r s A l l a n M u n c k Continued to page 18 NEWS & FEATURES TOP STORIES PEOPLE EVENTS

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